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Home | Alpha Telephone | Domain Names | Web Hosting | Get Traffic | xrEvidence | xrSoccer United States Patent
Redox systems for brain-targeted drug delivery Inclusion complexes of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrin with the reduced, biooxidizable, blood-brain barrier penetrating, lipoidal forms of dihydropyridine.revreaction.pyridinium salt redox systems for brain-targeted drug delivery provide a means for stabilizing the redox systems, particularly against oxidation. The redox inclusion complexes also provide a means for decreasing initial drug concentrations in the lungs after administration of the systems, leading to decreased toxicity. In selected instances, complexation results in substantially improved water solubility of the redox systems as well.
Primary Examiner: Griffin; Ronald W. Attorney, Agent or Firm: CROSS-REFERENCE TO RELATED APPLICATIONS This application is a continuation-in-part of applicant's copending application Ser. No. 07/139,755, filed Dec. 30, 1987, and of applicant's copending application Ser. No. 07/174,945, filed Mar. 29, 1988. Ser. No. 07/174,945 is itself a continuation-in-part of Ser. No. 07/139,755. Both of said copending applications are incorporated by reference herein in their entirety and relied upon. What is claimed is: 1. A method for stabilizing the reduced, biooxidizable, blood-brain barrier penetrating, lipoidal dihydropyridine form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery, said method comprising complexing said dihydropyridine form with cyclodextrin selected from the group consisting of hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.-cyclodextrin and hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .tau.-cyclodextrin. 2. A method according to claim 1, wherein said dihydropyridine form is a compound of the formula wherein [D] is a centrally acting drug species and [DHC] is the reduced, biooxidizable, blood-brain barrier penetrating, lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox carrier. 3. A method according to claim 2 wherein the centrally acting drug species is a dopaminergic agent, an androgenic agent, an anticonvulsant, an anxiolytic agent, a neurotransmitter, an antibiotic or antibacterial agent, an antidepressant, an antiviral agent, an anticancer or antitumor agent, an antiinflammatory agent, an estrogen or a progestin. 4. A method according to claim 3, wherein the centrally acting drug species is dopamine, testosterone, phenytoin, GABA, valproic acid, tyrosine, methicillin, oxacillin, benzylpenicilli, cloxacillin, dicloxacillin, desipramine, acyclovir, trifluorothymidine, zidovuidine, hydroxy-CCNU, chlorambucil, tryptamine, dexamethasone, hydrocortisone, ethinyl estradiol, norethindrone, estradiol, ethisterone, norgestrel, estrone, estradiol 3-methyl ether, estradiol benzoate, norethynodrel, mestranol, indomethacin, naproxen, FENU, HENU or 5-FU. 5. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-{(N-{.beta.-[3,4-bis(pivalyloxy)phenyl] ethyl}carbamoyl}}-1,4-dihydropyridine, 1-methyl-3-{N-[[.beta.-[3,4-bis(isobutyryloxy)phenyl] ethyl]]}carbamoyl-1,4-dihydropyridine or N-{.beta.-[3,4-bis(pivalyloxy)phenyl]ethyl}aminocarbonyloxymethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 6. A method according to claim 4, wherein the compound of the formula [D-DHC] is 17.beta.-[(1,4-dihydro-1-methyl-3-pyridinylcarbonyl)oxy] androst-4-en-3-one or 17.beta.-{[(3"-carbamoyl-1',4'-dihydropyridinyl)acetyl]-oxy}androst-4-en-3 -one. 7. A method according to claim 4, wherein the compound of the formula [D-DHC] is 5,5-diphenyl-3-[(1'-methyl-1',4'-dihydropyridin-3'-yl) carbonyloxymethyl]-2,4-imidazolidinedione, 3-[(3'-carbamoyl-1',4'-dihydropyridin-1'-yl)acetyloxymethyl] -5,5-diphenyl-2,4-imidazolidinedione or 3-[3'-(3"-carbamoyl-1",4"-dihydropyridin-1"-yl)propionyloxymethyl] -5,5-diphenyl-2,4-imidazolidinedione. 8. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[3-(benzyloxycarbonyl)propyl] carbamoyl-1,4-dihydropyridine or 1-methyl-3-{N-[(3'-cyclohexylcarbonyl)propyl]}-carbamoyl-1,4-dihydropyridi ne. 9. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-[2'-(2"-propyl)pentanoyloxy] ethylcarbamoyl-1,4-dihydropyridine, 1-methyl-3-[2'-(2"-propyl)pentanoyloxy]ethoxycarbonyl1,4-dihydropyridine or 1-[2'-(2"-propyl)pentanoyloxy]-ethyl-3-carboxamide-1,4-dihydropyridine. 10. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-{N-[1'-ethoxycarbonyl)-2'-(4"-pivaloyloxyphenyl )ethyl] }-carbamoyl-1,4-dihydropyridine or 1-methyl-3-{N-[(1'-ethoxycarbonyl)-2'-(4"-isobutyryloxyphenyl)ethyl]}-carb amoyl-1,4-dihydropyridine. 11. A method according to claim 4, wherein the compound of the formula [D-DHC] is [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]-3,3-dimethyl-7-oxo-6-[(2,6-dimethoxy)benz amido] -4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.5.alpha.,6.beta.)-3,3-dimethyl-6-(5-methyl-3-phenyl-4-isoxazo lecarboxamido)-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.6.beta.)]-3,3-dimethyl-7-oxo-6-[(phenylacetyl)amino] -4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S(2.alpha.,5.alpha.,6.beta.)] -6-[3-(2-chlorophenyl)-5-methyl-4-isoxazolecarboxamidol-3,3-dimethyl-7-oxo -4-thia-1-aza bicyclo[3.2.0]heptane-2-carboxylate or [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]6[ 3-(2,6-dichlorophenyl)-5-methyl-4-isoxazolecarboxamido] -3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0] heptane-2-carboxylate. 12. A method according to claim 4, wherein the compound of the formula [D-DHC] is [{N-[3-(10,11-dihydro-5h-dibenz[b,f] azepin-5-yl)]propyl-N-methlamino}carbonyloxy] methyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate or [1-{N-[3-(10,11-dihydro-5H-dibenz[b,f] azepin-5-yl)]propyl-N-methylamino}carbonyloxy] ethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 13. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-{[2-(9-guanylmethoxy)ethoxy] carbonyl}-1,4-dihydropyridine. 14. A method according to claim 4, wherein the compound of the formula [D-DHC] is 3'-(1,4-dihydro-1methyl-3-pyridinylcarbonyl)-5'-pivaloyltrifluorothymidine . 15. A method according to claim 4, wherein the compound of the formula [D-DHC] is 3'-azido-3'-deoxy5'-(1-methyl-1,4-dihydro-3-pyridinyl)carbonyl] thymidine. 16. A method according to claim 4, wherein the compound of the formula [D-DHC] is N-(2-chloroethyl)N'-[4-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy) cyclohexyl]-N-nitrosourea, N-(2-fluoroethyl)-N'-[2-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy)ethyl] -N-nitrosourea or N-(2-chloroethyl)-N'-[2-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy)ethyl] -N-nitrosourea. 17. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-[(N-{2-[4-({4-[bis(2-chloroethyl)] amino}phenyl)butanoyloxy]ethyl})carbamoyl] -1,4-dihydropyridine, 1-methyl-3-(N-{4-[4-(4-{[bis(2-chloroethyl)] amino}phenyl)butanoyloxy] cyclohexyl)}carbamoyl)-1,4-dihydropyridine, 1-methyl-3-[(N-{2-[4-({4-bis(2-chloroethyl)] amino}phenyl)butanoyloxy] propyl})carbamoyl]-1,4dihydropyridine, 1-methyl-3-[(N-{2-phenyl-2-({4-[bis(2-chloroethyl)] amino}phenyl)butanoyloxy]}ethyl)carbammoyl] -1,4-dihydropyridine or 1-methyl-3-[N-({1-[4-(4-{[bis(2-chloroethyl)] amino}phenyl)butanoyloxy]cyclohexyl}methyl)carbamoyl] -1,4-dihydropyridine. 18. A method according to claim 4, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[2-(3-indolyl)ethyl] carbamoyl-1,4-dihydropyridine. 19. A method according to claim 4, wherein the compound of the formula [D-DHC] is 9-fluoro-11.beta.,17-dihydroxy-16.alpha.-methyl-21-{[(1-methyl-1,4-dihydro pyridin3-yl)carbonyl] oxy}pregna-1,4-diene-3,20-dione or 11.beta.,17-dihydroxy-21-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}pregn-4-ene-3,20-dione. 20. A method according to claim 4, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-[(1-methyl-1,4-dihydropyridin-3yl)carbonyl] oxyestra-1,3,5(10)-triene. 21. A method according to claim 4, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-{[1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10-triene-20-yne, 3-[(1-methyl-1,4-dihydro-3-pyridinyl)carbonyloxy] estra-1,3,5(10)-trien17-one, 17.beta.-[(1-methyl-1,4-dihydro-3-pyridinyl)carbonyloxy] estra-1,3,5(10)-trien-3-ol 3-methyl ether, 3,17.beta.-bis-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}estra-1,3,5(10)-triene, 3-(phenylcarbonyloxy)-17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl) carbonyl] oxy}estra-1,3,5(10)-triene or 3-methoxy-17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10)-trien-20-yne. 22. A method according to claim 4, wherein the compound of the formula [D-DHC] is 17.beta.-}[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-norpregn-4-en-20-yn-3-one, 17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}pregn-4-en-20-yn-3-one, 13-ethyl-17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl ] oxy}-18,19-dinorpregn-4-en-20-yn-3-one or 17.beta.-{[(1-methyl-1,4-dihydropyridin-3yl)carbonyl] oxy}-19-norpregn-5(10)-en-20-yn-3-one. 23. A method according to claim 4 wherein the compound of the formula [D-DHC] is 1-methyl-3-[N-(2-{1-(p-chlorobenzoyl)-5-methoxy-2-methyl-3-indoyl] -acetoxy}ethyl)carbamoyl]-1,4-dihydropyridine or 1-methyl-3-{N-[2-(6-methoxy-.alpha.-methyl-2-naphthalenylacetoxy)ethyl] carbamoyl-1,4-dihydropyridine. 24. A method according to claim 4, wherein the compound of the formula [D-DHC] is 3-(1,4-dihydro-1-methyl-3-pyridinylcarbonyloxymethyl)-5-fluorouracil or 1-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxymethyl-5-fluorouracil. 25. A method for decreasing initial lung concentrations of drug resulting from administration of the reduced, booxidizable, blood-brain barrier penetrating, lipoidal dihydropyridine form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery, said method comprising administering said dihydropyridine form as its inclusion complex with cyclodextrin selected from the group consisting of hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.-cyclodextrin and hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .tau.-cyclodextrin. 26. A method according to claim 25, wherein said dihydropyridine form is a compound of the formula wherein [D] is a centrally acting drug species and [DHC] is the reduced, booxidizable, blood-brain barrier penetrating, lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox carrier. 27. A method according to claim 26, wherein the centrally acting drug species is a dopaminergic agent, an androgenic agent, an anticonvulsant, an anxiolytic agent, a neurotransmitter, an antibiotic or antibacterial agent, an antidepressant, an antiviral agent, an anticancer or antitumor agent, an antiinflammatory agent, an estrogen or a progestin. 28. A method according to claim 27, wherein the centrally acting drug species is dopamine, testosterone, phenytoin, GABA, valproic acid, tyrosine, methicillin, oxacillin, benzylpenicillin, cloxacillin, dicloxacillin, desipramine, acyclovir, trifluorothymidine, zidovudine, hydroxy-CCNU, chlorambucil, tryptamine, dexamethasone, hydrocortisone, ethinyl estradoiol, norethindrone, estradiol, ethisterone, norgestrel, entrone, estradiol 3-methyl ether, estradiol benzoate, norethynodrel, mestranol, indomethacin, naproxen, FENU, HENU or 5-FU. 29. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-{{N-{.beta.-[3,4-bis(dipivalyloxy)phenyl] ethyl}carbamoyl}}-1,4-dihydropyridine, 1-methyl-3-{N-[[.beta.-[3,4-bis(isobutyryloxy)phenyl] ethyl]]}carbamoyl-1,4-dihydropyridine or N-{.beta.-[3,4-bis(pivalyloxy)phenyl]-ethyl}aminocarbonyloxymethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 30. A method according to claim 28, wherein the compound of the formula [D-DHC] is 17.beta.-[(1,4-dihydro-1-methyl-3-pyridinylcarbonyl)oxy]androst-4-en-3-one or 17.beta.-}[(3"-carbamoyl-1',4"-dihydropyridinyl)acetyl]-oxy}androst-4-en-3 -one. 31. A method according to claim 28, wherein the compound of the formula [D-DHC] is 5,5-diphenyl-3-[(1'-methyl-1',4'-dihydropyridin-3'-yl(carbonyloxymethyl] 2,4-imidazolidinedione, 3-[(3'-carbamoyl-1',4'-dihydropyridin-1'-yl)acetyloxymethyl] -5,5-diphenyl-2,4-imidazolidinedione or 3-[3'-(3"-carbamoyl-1",4"-dihydropyridin-1"-yl)propionyloxymethyl] -5,5-diphenyl-2,4-imidazolidinedione. 32. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[3-(benzyloxycarbonyl)propyl] carbamoyl-1,4-dihydropyridine or 1-methyl-3-{N-[(3'-cyclohexylcarbonyl)propyl[}-carbamoyl-1,4-dihydropyridi ne. 33. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-[2'-(2"-propyl)pentanoyloxy] ethylcarbamoyl-1,4-dihydropyridine, 1-methyl-3[2'-(2"-propyl)pentanoyloxy]ethoxycarbonyl-1,4-dihydropyridine or 1-[2'-(2"-propyl)pentanoyloxy] -ethyl-3-carboxamide-1,4-dihydropyridine. 34. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-{N-[(1'-ethoxycarbonyl)-2'-(4"-pivaloyloxyphen yl)ethyl]}-carbamoyl-1,4-dihydropyridine or 1-methyl-3-{N-[(1'-ethoxycarbonyl)-2'-(4"-isobutyryloxyphenyl)ethyl] }-carbamoyl-1,4-dihydropyridine. 35. A method according to claim 28, wherein the compound of the formula [D-DHC] is [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]-3,3-dimethyl-7-oxo-6-[(2,6-dimethoxy)benz amido] -4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)-3,3-dimethyl-6-(5-methyl-3-phenyl-4-isoxaz olecarboximido)-7-oxo-4-thia-1-azabicyclo[3.2.0]-heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]-3,3-dimethyl-7-oxo-6-[(phenylacetyl)amino ] -4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [[2S-(2.alpha.,5.alpha.,6.beta.)]-6-[3-(2-chlorophenyl)-5-methyl-4-isoxazo lecarboxamido ] -3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate or [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxo]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]-6-[3-(2,6-dichlorophenyl)-5-methyl-4-isox azolecarboxamido ] -3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate. 36. A method according to claim 28, wherein the compound of the formula [D-DHC] is [{N-[3-(10,11-dihydro-5H-dibez[b,f] azepin-5-yl)]propyl-N-methylamino}carbonyloxy] methyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate or [1-{N-[3-(10,11-dihydro-5H-dibenz[b,f] azepin-5yl)]propyl-N-methylamino}carbonyloxy] ethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 37. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-{[2-(9-guanylmethoxy)ethoxy] carbonyl}-1,4-dihydropyridine. 38. A method according to claim 28, wherein the compound of the formula [D-DHC] is 3'-(1,4-dihydro-1-methyl-3-pyridinylcarbonyl)-5'-pivaloyltrifluoro thymidine. 39. A method according to claim 28, wherein the compound of the formula [D-DHC] is 3'-azido-3'-deoxy-5'-(1-methyl-1,4-dihydro-3-pyridinyl)carbonyl] thymidine . 40. A method according to claim 28, wherein the compound of the formula [D-DHC] is N-(2-chloroethyl)-N'-[4-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy )-cyclohexyl] -N-nitrosourea, N-(2-fluoroethyl)-N'-[2-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy)ethyl] -N-nitrosourea or N-(2-chloroethyl)-N'-[2-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy)ethyl] -N-nitrosourea. 41. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-[(N-{2-[4-({4[bis(2-chloroethyl)] amino}phenyl)butanoyloxy]-ethyl})carbamoyl] -1,4-dihydropyridine, 1-methyl-3-(N-{4-[4-(4-{[bis(2-chloroethyl)] amino}phenyl)butanoyl-oxy] cyclohexyl}carbamoyl)-1,4-dihydropyridine, 1-methyl-3-[(N-{2[4-({4-bis(2-chloroethyl)] amino}-phenyl)butanoyloxy]cyclohexyl}-methyl)carbamoyl] -1,4-dihydropyridine. 42. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[2-(3-indolyl)ethyl] carbamoyl-1,4-dihydropyridine. 43. A method according to claim 28, wherein the compound of the formula [D-DHC] is 9-fluoro-11.beta.,17-dihydroxy-16.alpha.-methyl-21-{[(1-methyl-1,4-dihydro pyridin-3yl)carbonyl] oxy}pregna-1,4-diene-3,20-dione or 11.beta.,17-dihydroxy-21-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}pregn-4-ene-3,20-dione. 44. A method according to claim 28, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxyestra-1,3,5(10)-triene. 45. A method according to claim 28, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-}[1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10)-trien-20-yne, 3-[(1-methyl-1,4-dihydro-3-pyridinyl)carbonyloxy] estra-1,3,5(10)-trien-17-one, 17.beta.-[(1-methyl-1,4-dihydro-3-pyridinyl)-carbonyloxy] estra-1,3,5(10)-trien-3-ol 3-methyl ether, 3,17.beta.-bis-{[(1-methyl-1,4-dihydropyridin3-yl)carbonyl] oxy}estra-1,3,5(10)-triene, 3-(phenylcarbonyloxy)-17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl) -carbonyl]oxy}estra-1,3,5(10)-triene or 3-methoxy-17.beta.-}[1-methyl-1,4-dihydropyridin-3-yl )carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10)-trien-20-yne. 46. A method according to claim 28, wherein the compound of the formula [D-DHC] is 17.beta.-}[(1-methyl-1,4-dihydropyridin-3yl)carbonyl] oxy}-19-norpregn-4-en-20-yn-3-one, 17.beta.-{[(1-methyl-1,4-dihydropyridin-3yl)-carbonyl] oxy}pregn-4-en-20-yn-3-one, 13-ethyl-17.beta.-{[(1-methyl-1,4-dihydropyridin-3yl)carbonyl] oxy}-18,19-dinorpregn-4-en-20-yn-3-one or 17.beta.-{[(1-methyl-1,4-dihydropyridin-3yl)carbonyl]oxy}-19-norpregn-5(10 )-en-20-yn -3-one. 47. A method according to claim 28, wherein the compound of the formula [D-DHC] is 1-methyl-3-[N-(2-{1-(p-chlorobenzoyl)-5-methoxy-2-methyl-3 -indolyl] -acetoxy}ethyl)carbamoyl]-1,4-dihydropyridine or 1-methyl-3-{N-[2-(6-methoxy-.alpha.-methyl-2-naphthalenyl-acetoxy)ethyl] carbamoyl-1,4-dihydropyridine. 48. A method according to claim 28, wherein the compound of the formula [D-DHC] is 3-(1,4-dihydro-1-methyl-3-pyridinylcarbonyloxymethyl)-5-fluorouracil or 1-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxymethyl)-5-fluorouracil. 49. A method for decreasing the tendency of the reduced, biooxidizable, blood-brain barrier penetrating, lipoidal dihydropyridine form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery to provide high initial concentrations of drug in the lungs following administration, said method comprising complexing said dihydropyridine form with cyclodextrin selected from the group consisting of hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.-cyclodextrin and hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .tau.-cyclodextrin prior to administration. 50. A method according to claim 49 wherein said dihydropyridine form is a compound of the formula wherein [D] is a centrally acting drug species and [DHC] is the reduced, biooxodizable, blood-brain barrier penetrating, lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox carrier. 51. A method according to claim 30, wherein the centrally acting drug species is a dopaminergic agent, an androgenic agent, an anticonvulsant, an anxiolytic agent, a neurotransmitter, an antibiotic or antibacterial agent, an antidepressant, an antiviral agent, an anticancer or antitumor agent, an antiinflammatory agent, an estrogen or a progestin. 52. A method according to claim 51, wherein the centrally acting drug species is dopamine, testosterone, phenytoin, GABA, valproic acid, tyrosine, methicillin, oxacillin, benzylpenicillin, cloxacillin, dicloxacillin, desipramine, acyclovir, trifluorothymidine, zidovudine, hydroxy-CCNU, chlorambucil, tryptamine, dexamethasone, hydrocortisone, ethinyl estradiol, norethindrone, estradiol, ethisterone, norgestrel, estrone, estradiol 3-methyl ether, estradiol benzoate, norethynodrel, mestranol, indomethacin, naproxen, FENU, HENU or 5-FU. 53. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-}}N-}.beta.-[3,4-bis(pivalyloxy)phenyl] ethyl}carbamoyl}}-1,4-dihydropyridine, 1-methyl-3-{N-[[.beta.-[3,4-bis(isobutyryloxy)phenyl] ethyl]]}carbamoyl-1,4-dihydropyridine or N-{.beta.-[3,4-bis(pivalyloxy)phenyl]ethyl}aminocarbonyloxymethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 54. A method according to claim 52, wherein the compound of the formula [D-DHC] is 17.beta.-[(1,4-dihydro-1-methyl-3-pyridinylcarbonyl)oxy] androst-4-en-3-one or 17.beta.-{[(3"-carbamoyl-1',4"-dihydropyridinyl)acetyl]-oxy}androst-4-en-3 -one. 55. A method according to claim 52, wherein the compound of the formula [D-DHC] is 5,5-diphenyl-3-[(1'-methyl-1',4'-dihydropyridin-3'-yl)carbonyloxymethyl] -2,4-imidazolidinedione, 3-[(3'-carbamoyl-1',4'-dihydropyridin-1'-yl)acetyloxymethyl] -5,5-diphenyl-2,4-imidazolidinedione or 3-[3'-(3"-carbamoyl-1",4"-dihydropyridin-1"-yl)propionyloxymethyl] -5,5-diphenyl-2,4imidazolidinedione. 56. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[3-(benzyloxycarbonyl)propyl] carbamoyl-1,4-dihydropyridine or 1-methyl-3-N-[(3'-cyclohexylcarbonyl)propyl]}-carbamoyl-1,4-dihydrooyridin e. 57. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-[2'-(2"-propyl)pentanoyloxy] ethylcarbamoyl-1,4-dihydropyridine, 1-methyl-3-[2'-(2"-propyl)pentanoyloxy]ethoxycarbonyl-1,4-dihydropyridine or 1-[2'-(2"-propyl)pentanoyloxy]-ethyl-3-carboxamide-1,4-dihydropyridine. 58. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-{N-[(1'-ethoxycarbonyl)-2'-(4"-pivaloyloxypheny l)ethyl] }-carbamoyl-1,4-dihydropyridine or 1-methyl-3-{N-[(1'-ethoxycarbonyl)-2'-(4"-isobutyryloxy phenyl)ethyl] }-carbamoyl-1,4-dihydropyridine. 59. A method according to claim 52, wherein the compound of the formula [D-DHC] is [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2-(2.alpha.,5.alpha.,6.beta.)]-3,3-dimethyl-7-oxo-6-F-(2,6-dimethoxy) benzamido] -4-thia-1-azabicyclo[3.2.0] heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S(2.alpha.,5.alpha.,6.beta.)-3,3-dimethyl-6-(5-methyl-3-phenyl-4-isoxazo lecarboxamido)-7 oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)]-3,3-dimethyl-7-oxo-6-[(phenylacetyl)amino ] -4-thia-1azabicyclo[3.2.0]heptane-2-carboxylate, [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S(2.alpha.,5.alpha.,6.beta.)] -6-[3-(2-chlorophenyl)-5-methyl-4-isoxazolecarboxamido] -3,3-dimethyl-7-oxo-4-thia-1-azabicyclo-3.2.0]heptane-2-carboxylate or [[(1,4-dihydro-1-methyl-3-pyridinyl)carbonyl] oxy]methyl [2S-(2.alpha.,5.alpha.,6.beta.)] -6-[-3-(2,6-dichlorophenyl)-5-methyl-4-isoxazolecarboxamido] -3,3-dimethyl-7-oxo-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylate. 60. A method according to claim 52, wherein the compound of the formula [D-DHC] is [{N-[3-(10,11-dihydro-5H-dibenz[b,f] azepin-5-yl)]propyl-N-methylamino}carbonyloxy] methyl 1,4-dihydro-1-methyl-3pyridinecarboxylate dibenz[b,f]-lazepin-5-yl)]propyl-N-methylamino}carbonyl-oxy] ethyl 1,4-dihydro-1-methyl-3-pyridinecarboxylate. 61. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-{[2-(9-guanylmethoxy)ethoxy] carbonyl}-1,4-dihydropyridine. 62. A method according to claim 52, wherein the compound of the formula [D-DHC] is 3'-(1,4-dihydro-1-methyl-3-pyridinylcarbonyl)-5'-pivaloyltrifluoro thymidine. 63. A method according to claim 52, wherein the compound of the formula [0-DHC] is 3'-azido-3'-deoxy-5'-(1-methyl-1,4-dihydro-3-pyridin yl)carbonyl] thymidine. 64. A method according to claim 52, wherein the compound of the formula [D-DHC] is N-(2-chloroethyl)-N'-[4-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy )ethyl] -N-nitrosourea or N-(2-fluoroethyl)-N'-[2-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxy)ethyl] -N-nitrosourea. 65. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-[(N-{2[ 4-({4-[bis(2-chloroethyl)] amino}phenyl)butanoyloxy]-ethyl})carbamoyl]-1,4-dihydropyridine, 1-methyl-3-(N-4-[4-(4-[bis(2-chloroethyl)] amino}phenyl)butanoyloxy] cyclohexyl}carbamoyl)-1,4-dihydropyridine, 1-methyl-3-[(N-{2-[4-({4-bis(2-chloroethyl)] amino}phenyl)butanoyloxy] cyclohexyl}-methyl)carbamoyl]-1,4-dihydropyridine. 66. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-N-[2-(3-indolyl)ethyl] carbamoyl-1,4-dihydropyridine. 67. A method according to claim 52, wherein the compound of the formula [D-DHC] is 9-fluoro-11.beta.,17-dihydroxy-16.alpha.-methyl-21-}[(1-methyl-1,4-dihydro pyridin-3-yl)carbonyl] oxypregna-1,4-diene-3,20-dione or 11.beta.,17-dihydroxy-21-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}pregn-4-ene-3,20-dione. 68. A method according to claim 52, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxyestra-1,3,5(10)-triene. 69. A method according to claim 52, wherein the compound of the formula [D-DHC] is 3-hydroxy-17.beta.-}[1-methyl-1,4-dihydrooyridin-3-yl)carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10-trien-20-yne, 3-[(1-methyl-1,4-dihydro-3-pyridinyl)carbonyloxy] estra-1,3,5(10)-trien17-one, 17.beta.-[(1-methyl-1,4-dihydro-3-pyridinyl)-carbonyloxy] estra-1,3,5(10)-trien-3-ol 3-methyl ether, 3,17.beta.-bis-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}estra-1,3,5(10)-triene or 3-methoxy-17.beta.-{[1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-nor-17.alpha.-pregna-1,3,5(10)-trien-20-yne. 70. A method according to claim 52, wherein the compound of the formula [D-DHC] is 17.beta.-{[(1-methyl-1,4-dihydropyridin-3yl)carbonyl] oxy}-19-norpregn-4-en-20-yn-3-one, 17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)-carbonyl] oxy}pregn-4-en-20yn-3-one, 13ethyl-17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-18,19-dinorpregn-4-en-20-yn-3-one or 17.beta.-{[(1-methyl-1,4-dihydropyridin-3-yl)carbonyl] oxy}-19-norpregn-5(10)-en-20-yn-3-one. 71. A method according to claim 52, wherein the compound of the formula [D-DHC] is 1-methyl-3-[N-(2-{1-(p-chlorobenzoyl)-5-methoxy-2-methyl-3-indoyl] -acetoxy}ethyl)carbamoyl]-1,4-dihydropyridine or 1-methyl-3-{N-[2-(6-methoxy-.alpha.-methyl-2-naphthalenylacetoxy)ethyl] carbamoyl-1,4-dihydropyridine. 72. A method according to claim 52, wherein the compound of the formula [D-DHC] is 3-(1,4-dihydro-1-methyl-3-pyridinylcarbonyloxymethyl)-5-fluorouracil or 1-(1,4-dihydro-1-methyl-3-pyridinecarbonyloxymethyl)-5-fluorouracil. FIELD OF THE INVENTION The present invention provides a method for stabilizing the reduced, dihydropyridine forms of dihydropyridine .revreaction. pyridinium salt redox systems for brain-targeted drug delivery by forming inclusion complexes of the dihydropyridine forms with selected cyclodextrins. These redox inclusion complexes also provide a means for increasing the ratio of initial brain to lung concentrations, thus leading to decreased toxicity. In selected instances, complexation results in substantially improved water solubility of the redox systems as well. BACKGROUND OF THE INVENTION Cyclodextrins are cyclic oligosaccharides. The most common cyclodextrins are .alpha.-cyclodextrin, which is composed of a ring of six glucose residues; .beta.-cyclodextrin, which is composed of a ring of seven glucose residues; and Y-cyclodextrin, which is composed of a ring of eight glucose units. The inside cavity of a cyclodextrin is lipophilic, while the outside of the cyclodextrin is hydrophilic; this combination of properties has led to widespread study of the natural cyclodextrins, particularly in connection with pharmaceuticals, and many inclusion complexes have been reported. .beta.-Cyclodextrin has been of special interest because of its cavity size, but its relatively low aqueous solubility (about 1.8% w/v at 25.degree. C.) and attendant nephrotoxicity has limited its use in the pharmaceutical field. Attempts to modify the properties of the natural cyclodextrins have resulted in the development of heptakis (2,6-di-0-methyl)-.beta.-cyclodextrin, heptakis (2,3,6-tri-0-methyl)-.beta.-cyclodextrin, hydroxypropyl-.beta.-cyclodextrin, .beta.-cyclodextrin-epichlorohydrin polymer and others. For a comprehensive review of cyclodextrins and their use in pharmaceutical research, see Pitha et al, in Controlled Drug Delivery, ed. S. D. Bruck, Vol. I, CRC Press, Boca Raton, Fla. pp. 125- 148 (1983). For an even more recent overview, see Uekama et al, in CRC Critical Reviews in Therapeutic Drug Carrier Systems, Vol. 3 (1), 1-40 (1987); Uekama, in Topics in Pharmaceutical Sciences 1987, eds. D. D. Breimer and P. Speiser, Elsevier Science Publishers B.V. (Biomedical Division), 181-194 (1987); and Pagington, Chemistry in Britain, pp. 455-458 (May 1987). Inclusion complexes of .alpha.-, .beta.- or .gamma.-cyclodextrin or their mixtures with a variety of drugs have been described by numerous parties and various advantages have been attributed to the complexes. These descriptions include the following: __________________________________________________________________________ U.S. ACTIVE INVENTOR PAT. NO. INGREDIENT USE ADVANTAGE __________________________________________________________________________ Noda et al 4,024,223 menthol &/or antiphlogistic, reduced unpleasant methyl analgesic odor, increased salicylate wet packing effect Szejtli et al 4,228,160 indomethacin anti-inflam- reduced ulcerative matory, pro- effect tective during pregnancy Hayashi et al 4,232,009 .omega.-halo-PGI.sub.2 hypotensive, increased stability analogs uterine con- traction stimulating, blood platelet aggregation inhibiting Matsumoto et al 4,351,846 3-hydroxy- and uterine contrac- increased stability 3-oxo- tion stimulating prostagiandin analogs Yamahira et al 4,352,793 bencyclane anticonvulsant, increased stability fumarate vasodilative at strong acid pH, faster gastric emptying, higher blood concentra- tions, less irritation improved hemolytic activity Lipari 4,383,992 steroids-- hormonal improved water corticosteroids solubility, increased androgens, therapeutic response anabolic in eye steroids, estrogens, progestagens Nicolau 4,407,795 p-hexadecyl- antiathero- enhanced aminobenzoic sclerotic bioavailability acid sodium salt Tuttle.sup.1 4,424,209 3,4-diisobutyr- cardiac yioxy-N-[3-(4- contractility isobutyryloxy- agent phenyl)-1- methyl-n- propyl]-.beta.- phenethylamine Tuttle 4,425,336 3,4-dihydroxy- cadiac capable of oral N-[3-(4-hydroxy- contractility administration phenyl)-1- agent methyl-n- propyl]-.beta.- phenethylamine Wagu et al 4,438,106 EPA and DHA deodorized (fatty acids) storage stable Masuda et al.sup.2 4,474,811 2-(2-fluoro-4- anti- reduced eye biphenylyl)pro- inflammatory irritation, pionic acid ophthalmic higher concen- or salt trations, no side effects, highly soluble, long stability, excellent pharmacological effects Shinoda et al 4,478,995 acid addition anti-ulcer excellent water salt of (2'- solubility, good benzyloxycar- absorption in diges- bonyl)phenyl tive tract, good trans-4-guani- anti-ulcer activity dinomethylcyclo- hexanecarboxylate Hayashi et al 4,479,944 PGI.sub.2 analog for treatment of stabilization against artereosclerosis, decomposition cardiac failure or thrombosis Hayashi et al 4,479,966 6,9-methano- for hypertension, increased stability PGI.sub.2 analogs cerebral throm- bosis and the like Harada et al 4,497,803 lankacidin- antibiotic for enhanced water group antibiotic swine dysentery solubility and stability, increased rate and amount of absorption Masuda 4,499,085 prostaglandin treating anoxia analog of brain cells Szejtli et al 4,518,588 phendiline, i.e. coronary dilator improved water solu- N-(1-phenyl- calcium bility, accelerated ethyl)-3,3- antagonist and increased in diphenylpro- vivo resorption pylamine or its & dissolution at pH/ hydrochloride temperature of gastric acid Szejtli et al 4,524,068 piperonyl synergizes easily handled butoxide pesticidal effect crystalline solid; of known insecti- improved water solu- cides and fungi- bility, increased cides absorption & velocity of penetration through biological membranes Jones 4,555,504 a cardiac cardiac effect high aqueous solu- glycoside bility, apparently better bioavail- ability Uekama et al.sup.3 4,565,807 pirprofen anti-inflam- improved stability matory, to oxidation, analgesic, freedom from bitter antipyretic taste, less irritating Ueda et al 4,575,548 2-nitroxymethyl- for vascular non-volatile powder 6-chloropyridine disorders vs. volative oil Ohwaki et al.sup.4 4,598,070 tripamide anti-hyper- improved solubility tensive Chiesi et al 4,603,123 piroxicam, i.e. anti-inflam- 4-hydroxy-2- matory, analgesic methyl-N-2- pyridyl-2H-1,2- benzothiazine-3- carboxamide-1,1- dioxide Hasegawa et al 4,608,366 mobenzoxamine, antiemetic, storage stability i.e. 1-[2-(4- antispasmodic better absorption methoxybenzhy- through digestive dryloxy)ethyl]- tract 4-[3-(4-fluoro- benzoyl)propyl]- piperazine Hirai et al.sup.2 4,659,696 polypeptide improving drug absorption by non- oral and non- injection routes Szejtli et al 4,623,641 PGI.sub.2 methyl anti-ulcer improved storage ester stability Ninger et al 4,663,316 unsaturated antibiotic, enhanced stability phosphorus- antifungal, against oxidation containing antitumor antibiotics, including phosphotrienin Fukazawa et al 4,675,395 hinokitiol bactericidal, improved water solu- bacteriostatic bility, less odor Shimizu et al 4,728,509 2-amino-7- anti-allergic, improved water solu- isopropyl-5- anti- bility to increase oxo-5H-[1]- inflammatory concentration to benzopyrano- therapeutic levels [2,3-b]pyridine- in nasal drops and 3-carboxylic acid eye drops Shibanai et al.sup.6 4,728,510 a milk bath improved stability component preparation Karl et al 4,751,095 aspartame dipeptide stabilization from sweetener hydrolysis __________________________________________________________________________ .sup.1 Tuttle also describes use of 2,6di-O-methyl-cyclodextrin and 2,3,6tri-O-methyl cyclodextrin to form the inclusion complex. .sup.2 This may not be an inclusion complex, but simply a physical mixture. .sup.3 This is a mixture and/or an inclusion compound. .sup.4 The inventors also mention prior known solubility improvements of cyclodextrin inclusions of barbituric acid derivatives, mefenamic acid, indomethacin and chloramphenicol. .sup.5 The inventors refer to this as an "occlusion" compound. .sup.6 The inventors also mention a derivative of cyclodextrin and a cyclodextrincontaining starch decomposition product for use in forming th clathrate. Inclusion complexes of 2,6 -di-methyl-.beta.-cyclodextrin with dibenzo[bd]pyran derivatives and salts having analgesic, antemetic and narcosispotentiating activities have been described in Nogradi et al U.S. Pat. No. 4,599,327; increased water solubility and thus improved biological activity have been claimed for the complexes. A review of the pharmaceutical applications of such methylated cyclodextrins has been published by Uekama, Pharm Int., March 1985, 61-65; see also Pitha, Journal of Inclusion Phenomena 2, 477-485 (1984). Cyclodextrin polymer has been reported by Fenyvesi et al, Chem. Pharm. Bull. 32 (2), 665-669 (1984) to improve the dissolution of furosemide. Improvements in the dissolution and absorption of phenytoin using a water-soluble .beta.-cyclodextrin epichlorohydrin polymer have been described by Uekama et al, International Journal of Pharmaceutics, 23, 35-42 (1985). Hydroxypropyl-.beta.-cyclodextrin (HPCD) and its preparation by propylene oxide addition to .beta.-cyclodextrin were described in Gramera et al U.S. Pat. No 3,459,731 nearly 20 years ago. Gramera et al also described the analogous preparation of hydroxyethyl-.beta.-cyclodextrin by ethylene oxide reaction with .beta.-cyclodextrin. Much more recently, Pitha and co-workers have described the improved preparation of this cyclodextrin derivative and its effects on the dissolution of various drug molecules. Pitha U.S. Pat. No. 4,596,795, dated June 24, 1986, describes inclusion complexes of sex hormones, particularly testosterone, progesterone, and estradiol, with specific cyclodextrins, preferably hydroxypropyl-.beta.-cyclodextrin and poly-.beta.-cyclodextrin. The complexes enable the sex hormones to be successfully delivered to the systemic circulation via the sublingual or buccal route; the effectiveness of this delivery is believed to be due to "the high dissolution power of hydrophilic derivatives of cyclodextrins, the non-aggregated structure of their complexes with steroids, and their low toxicity and irritancy of mouth tissue". Success with other cyclodextrins, including poly-.gamma.-cyclodextrin and hydroxypropyl-.gamma.-cyclodextrin, have also been noted in the Pitha patent. See also Pitha et al, J. Pharm. Sci., Vol. 74, No. 9, 987-990 (September 1985), concerning the same and related studies. Pitha et al also describe in the J. Pharm. Sci. article the storage stability of tablets containing a testosterone-hydroxypropyl-.beta.-cyclodextrin complex and the lack of toxicity of the cyclodextrin itself, as well as the importance of the amorphous nature of the cyclodextrin derivatives and their complexes with drugs in improving dissolution properties. The improved, optimized preparation and purification of hydroxypropyl-.beta.-cyclodextrin has been recently described by Pitha et al, International Journal of Pharmaceutics 29, 73-82 (1986). In the same publication, the authors have described increased water solubility for 32 drugs in concentrated (40 to 50%) aqueous solutions of hydroxypropyl-.beta.-cyclodextrin; improved solubilization of acetaminophen, apomorphine, butylated hydroxytoluene, chlorthalidone, cholecalciferol, dexamethasone, dicumarol, digoxin, diphenylhydantoin, estradiol, estriol, ethinylestradiol-3-methyl ether, ethisterone, furosemide, hydroflumethiazide, indomethacin, iproniazid phosphate, 17-methyltestosterone, nitroglycerin, norethindrone, ouabain, oxprenolol, progesterone, retinal, retinoic acid (all trans and salt forms), retinol, spironolactone, sulpiride, testosterone and theophylline was noted. The authors indicated this to be an extension of their earlier work with hydroxypropyl-.beta.-cyclodextrin, which was previously found effective for oral administration of the sex hormones to humans. Their later work reported in Pitha et al, International Journal of Pharmaceutics 29, 73-82 (1986), has also been very recently described in Pitha U.S. Pat. No. 4,727,064, dated Feb. 23, 1988. That patent claims a composition containing an amorphous complex of cyclodextrin and a drug, and a method of producing a stabilizing amorphous complex of a drug and a mixture of cyclodextrins comprising (1) dissolving an intrinsically amorphous mixture of cyclodextrin derivatives which are water soluble and capable of forming inclusion complexes with drugs in water; and (2) solubilizing lipophilic drugs into aqueous media to form a solution and form a solubilized drug/cyclodextrin complex. The patent describes the preparation of various substituted amorphous cyclodextrins, including hydroxypropyl-.beta.-cyclodextrin and hydroxypropyl.gamma.-cyclodextrin, the latter by analogous condensation of propylene oxide and .gamma.-cyclodextrin. Uekama et al, CRC Critical Reviews in Therapeutic Drug Carrier Systems, Vol. 3 (1), pp. 1-40 (1987), have described the characteristics of various cyclodextrins, including hydroxypropyl-.beta.-cyclodextrin. The authors have presented data showing improved solubilization in water in the presence of 15 mg/mL of HPCD for the drugs carmofur, diazepam, digitoxin, digoxin, flurbiprofen, indomethacin, isosorbide dinitrate, phenytoin, prednisolone, progesterone and testosterone. In a discussion of the metabolism and toxicity of cyclodextrins, Uekama et al have indicated that cyclodextrins at sufficiently high concentrations cause hemolysis, and that the methylated cyclodextrins have higher hemolytic activity than the natural cyclodextrins. Hydroxypropyl-.beta.-cyclodextrin is said to cause hemolysis beginning at 4.5 mM. The authors have further indicated that parenteral administration of large doses of cyclodextrins should be avoided, but that ".gamma.-cyclodextrin and hydroxypropyl-.beta.-cyclodextrin seem to be useful in drug solubilization for injections and liquid preparations used for mucous membranes." JANSSEN PHARMACEUTICA N.V.'s International Patent Application No. PCT/EP84/00417, published under International Publication No. WO85/02767 on July 4, 1985, has described pharmaceutical compositions comprising inclusion compounds of drugs, which are unstable or only sparingly soluble in water, with partially etherified .beta.-cyclodextrin derivatives having hydroxyalkyl and optionally additional alkyl groups. Among the cyclodextrin derivatives contemplated are hydroxypropyl-.beta.-cyclodextrin and hydroxyethyl-.beta.cyclodextrin, while the drugs include non-steroidal anti-rheumatic agents, steroids, cardiac glycosides and derivatives of benzodiazepine, benzimidazole, piperidine, piperazine, imidazole and triazole. Preferred drugs include etomidate, ketoconazole, tubulazole, itraconazole, levocabastine and flunarizine. The pharmaceutical compositions of the invention include oral, parenteral and topical formulations, with 4 to 10% solutions of cyclodextrin derivatives being utilized to solubilize various drugs. Improved solubilities of indomethacin, digitoxin, progesterone, dexamethasone, hydrocortisone and diazepam using 10% HPCD are shown, and an injectable formulation of diazepam in 7% HPCD is specifically described. The relatively low cyclodextrin concentrations used reflect a desire to avoid or minimize the hemolytic effects observed at higher cyclodextrin concentrations. Japanese Kokai 88-218,663 (Kamikama et al) describes a pharmaceutical preparation containing nimodipine solubilized with hydroxypropyl-.beta.cyclodextrin. Carpenter et al, The Journal of Pediatrics, 111, 507-512 (October 1987) describe intravenous infusion of 2-hydroxypropyl-.beta.-cyclodextrin, prepared as a 5% solution in water, to treat severe hypervitaminosis A. It was found that, during infusion, circulating retinyl esters increased transiently, while total vitamin A excreted in the urine was enhanced after infusion. Thus, intravenous infusion of 5% HPCD was found to decrease in vivo levels of the vitamin, presumably by complexing with the vitamin and removing some of the excess from the body. The preparation of amorphous water-soluble cyclodextrin derivatives, including 2-hydroxyethyl-.beta.-cyclodextrin, 3-hydroxypropyl-.beta.-cyclodextrin and 2-hydroxypropyl-.gamma.-cyclodextrin, is described by Irie et al, Pharmaceutical Research, Vol. 5, No. 11, 1988, 713- 717. That report also addresses the distribution of the substituents among the glucose residues of the cyclodextrin ring. A pharmaceutical evaluation of hydroxyalkyl ethers of .beta.-cyclodextrins has been recently reported by Yoshida et al, International Journal of Pharmaceutics 46, 1988, 217-222. Aqueous solubilities, surface activities, hemolytic activity and local irritancy are reported. The data suggest that hydroxyalkyl-.beta.-cyclodextrins overcome many of the undesirable characteristics of .beta.-cyclodextrin usage in pharmaceuticals. JANSSEN PHARMACEUTICA N.V.'s European Patent Application No. 86200334.0, published under EPO Publication No. 0197571 on Oct. 15, 1986, describes .gamma.-cyclodextrin derivatives which are .gamma.-cyclodextrin substituted with C.sub.1 -C.sub.6 alkyl, hydroxy C.sub.1 -C.sub.6 alkyl, carboxy C.sub.1 -C.sub.6 alkyl or C.sub.1 -C.sub.6 alkyloxycarbonyl C.sub.1 -C.sub.6 alkyl or mixed ethers thereof. Among the specific derivatives named are hydroxypropyl-.gamma.-cyclodextrin and hydroxyethyl-.gamma.-cyclodextrin. Compositions comprising the cyclodextrin derivatives and a drug are also described. See also corresponding Muller U.S. Pat. No. 4,764,604, dated Aug. 16, 1988. The inclusion characteristics of yet other derivatized cyclodextrins have also been described in the literature. Studies of branched cyclodextrins which are glucosyl and maltosyl derivatives of .alpha.-, .beta.- and .gamma.-cyclodextrin and their inclusion complexes with drugs have recently been reported. Uekama, in Topics in Pharmaceutical Sciences 1987, eds. D. D. Breimer and P. Speiser, Elsevier Science Publishers B.V. (Biomedical Division), 181-194 (1987), has described the effects on biopharmaceutical properties of maltosyl and glucosyl cyclodextrin derivatives, as well as hydroxypropyl and other hydrophilic cyclodextrin derivatives, including enhanced drug absorption. The mechanism of enhancing drug absorption is described and the apparent stability constants for inclusion complexes of various drugs with .beta.-cyclodextrin, dimethyl-.beta.-cyclodextrin, hydroxypropyl-.beta.-cyclodextrin and maltosyl-.beta.-cyclodextrin are given. Drugs studied with these cyclodextrins include benoxaprofen, biphenyl acetic acid, carmofur, clofibrate, chlorpromazine, diazepam, diclofenac, digitoxin, digoxin, ethyl 4-biphenyl acetate, flurbiprofen, isosorbide dinitrate, indomethacin, menadione, nimodipine, nisoldipine, phenytoin, prednisolone, progesterone, prostacyclin, various prostaglandins (E.sub.1, E.sub.2, A.sub.1, A.sub.2), protriptyline, spironolactone and testosterone. Uekama also discussed the hemolytic effects of cyclodextrins. Summarizing the various studies using human erythrocytes, Uekama indicated that the natural cyclodextrins at relatively high concentrations caused hemolysis in the order .gamma. <.alpha.<.beta.. In the case of chemically modified cyclodextrins, the order changed to hydroxyethyl-.beta.< maltosyl-.beta.<hydroxypropyl-.beta.<.beta.. At relatively low concentrations, the cyclodextrins provided protection from hemolysis induced with various membrane-perturbing drugs, suggesting complexation as a means of reducing local toxicity of drugs: The natural cyclodextrins were found to reduce muscular tissue damage following intramuscular injection of drugs. Uekama concluded that the protective effects of cyclodextrins "are attributable to the poor affinity of the hydrophilic complex to muscular tissue membrane. The hydroxyethyl, hydroxypropyl, and glucosyl CyDs are more effective to reduce the local toxicity induced by drugs compared with natural CyDs, owing to the highly hydrophilic nature." Koizumi et al, Chem. Pharm. Bull. 35 (8), 3413- 3418 (1987), have reported on inclusion complexes of poorly water-soluble drugs with glucosyl cyclodextrins, namely 6-O-.alpha. -D-glucosyl-.alpha.-CD (G.sub.1 -.alpha.-CD), 6 -O-.alpha.-D-glucosyl-.beta.-CD (G.sub.1 -.beta.-CD) and 6A, 6.sup.D -di-O-.alpha.-D-glucosyl-.beta.-CD (2G.sub.1 -.beta.-D). Okada et al, Chem. Pharm. Bull., 36 (6), 2176-2185 (1988), have reported on the inclusion complexes of poorly water-soluble drugs with maltosyl cyclodextrins, namely 6 -O-.alpha.-maltosyl-.alpha.-CD (G.sub.2 -.alpha.-CD), 6 -O-.alpha.-maltosyl-.beta.-CD (G.sub.2 -.beta.-CD), 6 -O-.alpha.-maltosyl-.gamma.-CD (G.sub.2 -.gamma.-CD), 6 -O-.alpha.-maltotriosyl-.alpha.-CD (G.sub.3 -.alpha.-CD), 6 -O-.gamma.-maltotriosyl-.beta.-CD (G.sub.3 -.beta.-CD) and 6-0-.gamma.-maltotriosyl-.gamma.-CD (G.sub.3 -.gamma.-CD). Yamamoto et al, in International Journal of Pharmaceutics 49, 163-171 (1989), have described physicochemical properties of branched .beta.-cyclodextrins such as glucosyl-.beta.-cyclodextrin, maltosyl-.beta.-cyclodextrin and di-maltosyl-.beta.-cyclodextrin, and their inclusion characteristics. Those authors report that the branched .beta.-cyclodextrins are better solubilizers for poorly water-soluble drugs and have less hemolytic activity than .beta.-cyclodextrin itself, and they suggest that glucosyl-.beta.-cyclodextrin and maltosyl-.beta.cyclodextrin may be especially useful in parenteral preparations. The patent literature reflects much recent work on the branched cyclodextrins carried out by Japanese workers, as discussed below. Japanese Kokai 63-135402 (TOKUYAMA SODA KK), published June 7, 1988, describes compositions consisting of maltosyl-.beta.-cyclodextrin and at least one of digitoxin, nifedipine, flulubiprophene, isosorbide nitrate, phenytoin, progesterone or testosterone. The compositions have improved water solubility and reduced erythrocyte destruction, are safe for humans and can be used as injections, eye drops, syrups, and for topical and mucous membrane application. Japanese Kokai 62-281855 (DAIKIN KOGYO KK), published Dec. 7, 1987, describes stable, water-soluble inclusion compounds of maltosyl-.beta.-cyclodextrin with a variety of vitamins and hormones, e.g. steroid hormones such as prednisolone, hydrocortisone and estriol. These lipophilic vitamins and hormones can thus be used as aqueous solutions. Japanese Kokai 63-036793 (NIKKEN CHEM KK), published Feb. 17, 1988, describes the preparation of dimaltosyl-.gamma.-cyclodextrin and its general use in medicines. Japanese Kokai 62-106901 (NIKKEN CHEM KK), published May 18, 1987, describes the preparation of diglucosyl-.beta.-cyclodextrin and its general use for pharmaceuticals. Japanese Kokai 61-236802 (NIKKEN CHEM KK), published Oct. 22, 1986, describes the preparation of maltosyl-.gamma.-cyclodextrin and its general use with drugs. Japanese Kokai 61-197602 (NIKKEN CHEM KK), published Sept. 1, 1986, describes the preparation of maltosyl-.beta.-cyclodextrin and its expected use in medicines. Japanese Kokai 61-070996 (NIKKEN CHEM KK), published Apr. 11, 1986, describes the preparation of maltosyl-.alpha.-cyclodextrin and its general use in pharmaceuticals. Japanese Kokai 63-027440 (SANRAKU OCEAN), published Feb. 5, 1988, describes compositions containing a water-insoluble or slightly soluble drug together with glucosylated branched cyclodextrin. Among the drugs mentioned are steroid hormones. Japanese Kokai 62-164701 (SHOKUHIN SANGYO BIO), published July 21, 1987, describes the preparation of diglucosyl-.alpha.-cyclodextrin and its general use in medicine. Japanese Kokai 62-003795 (TOKUYAMA SODA KK), published Jan. 9, 1987, describes production of glucose and maltoligosaccharide (2-4 glucose units) derivatives of .alpha.-, .beta.- and .gamma.-cyclodextrin and their use as stabilizers for pharmaceuticals. The delivery of drugs to the brain is often seriously limited by transport and metabolism factors and, more specifically, by the functional barrier of the endothelial brain capillary wall, i.e. the bloodbrain barrier or BBB. Site-specific delivery and sustained delivery of drugs to the brain are even more difficult. A dihydropyridine .revreaction. pyridinium salt redox system has recently been successfully applied to delivery to the brain of a number of drugs. Generally speaking, according to this system, a dihydropyridine derivative of a biologically active compound is synthesized, which derivative can enter the CNS through the blood-brain barrier following its systemic administration. Subsequent oxidation of the dihydropyridine species to the corresponding pyridinium salt leads to delivery of the drug to the brain. Three main approaches have been published thus far for delivering drugs to the brain using this redox system. The first approach involves derivation of selected drugs which contain a pyridinium nucleus as an integral structural component. This approach was first applied to delivering to the brain N-methylpyridinium-2-carbaldoxime chloride (2-PAM), the active nucleus of which constitutes a quaternary pyridinium salt, by way of the dihydropyridine latentiated prodrug form thereof. Thus, a hydrophilic compound (2-PAM) was made lipoidal (i.e. lipophilic) by making its dihydropyridine form (Pro-2-PAM) to enable its penetration through lipoidal barriers. This simple prodrug approach allowed the compound to get into the brain as well as other organs, but this manipulation did not and could not result in any brain specificity. On the contrary, such approach was delimited to relatively small molecule quaternary pyridinium ring-containing drug species and did not provide the overall ideal result of brain-specific, sustained release of the desired drug, with concomitant rapid elimination from the general circulation, enhanced drug efficacy and decreased toxicity. No "trapping" in the brain of the 2-PAM formed in situ resulted, and obviously no brain-specific, sustained delivery occurred as any consequence thereof: the 2-PAM was eliminated as fast from the brain as it was from the general circulation and other organs. Compare U.S. Pat. Nos. 3,929,813 and 3,962,447; Bodor et al, J. Pharm. Sci, 67, No. 5, 685 (1978). See also Bodor, "Novel Approaches for the Design of Membrane Transport Properties of Drugs", in Design of Biopharmaceutical Properties Through Prodrugs and Analogs, Roche, E. B. (ed.), APhA Academy of Pharmaceutical Sciences, Washington, D.C., 98-135 (1976). Subsequent extension of this first approach to delivering a much larger quaternary salt, berberine, to the brain via its dihydropyridine prodrug form was, however, found to provide site-specific sustained delivery to the brain of that anticancer agent See Bodor et al, Science, Vol. 214, Dec. 18, 1981, 1370-1372. The second approach for delivering drugs to the brain using the redox system involves the use of a pyridinium carrier chemically linked to a biologically active compound. Bodor et al, Science, Vol. 214, Dec. 18, 1981, 1370-1372, outline a scheme for this specific and sustained delivery of drug species to the brain, as depicted in the following Scheme I: ##STR1## According to the scheme in Science, a drug [D] is coupled to a quaternary carrier [QC].sup.+ and the [D-QC].sup.+ which results is then reduced chemically to the lipoidal dihydro form [D-DHC]. After administration of [D-DHC] in vivo, it is rapidly distributed throughout the body, including the brain. The dihydro form [D-DHC] is then in situ oxidized (rate constant, k.sub.1) (by the NAD .revreaction. NADH system) to the ideally inactive original .sup.+ quaternary salt which, because of its ionic, hydrophilic character, should be rapidly eliminated from the general circulation of the body, while the blood-brain barrier should prevent its elimination from the brain (k.sub.3 >>k.sub.2; k.sub.3 >>k.sub.7). Enzymatic cleavage of the [D-QC].sup.+ that is "locked" in the brain effects a sustained delivery of the drug species [D], followed by its normal elimination (k.sub.5), metabolism. A properly selected carrier [OC].sup.+ will also be rapidly eliminated from the brain (k.sub. 6 >>k.sub.2). Because of the facile elimination of [D-QC].sup.+ from the general circulation, only minor amounts of drug are released in the body k.sub.3 >>k.sub.4); [D] will be released primarily in the brain (k.sub.4 >k.sub.2). The overall result ideally will be a brain-specific sustained release of the target drug species. Specifically, Bodor et al worked with phenylethylamine as the drug model That compound was coupled to nicotinic acid, then quaternized to give compounds of the formula ##STR2## which were subsequently reduced by sodium dithionite to the corresponding compounds of the formula ##STR3## Testing of the N-methyl derivative in vivo supported the criteria set forth in Scheme I. Bodor et al speculated that various types of drugs might possibly be delivered using the depicted or analogous carrier systems and indicated that use of N-methylnicotinic acid esters and amides and their pyridine ring-substituted derivatives was being studied for delivery of amino- or hydroxyl-containing drugs, including small peptides, to the brain. No other possible specific carriers were disclosed. Other reports of this work with the redox carrier system have appeared in The Friday Evening Post, Aug. 14, 1981, Health Center Communications, University of Florida, Gainesville, Fla.; Chemical & Engineering News, Dec. 21, 1981, pp. 24-25; and Science News, Jan. 2, 1982, Vol. 121, No. 1, page 7. More recently, the redox carrier system has been substantially extended in terms of possible carriers and drugs to be delivered. See International Patent Application No. PCT/US83/00725, filed May 12, 1983 and published Nov. 24, 1983 under International Publication No WO83/03968. Also see Bodor et al, Pharmacology and Therapeutics, Vol. 19, No. 3, 337-386 (1983); and Bodor U.S. Pat. No. 4,540,564, issued Sept. 10, 1985. The third approach for delivering drugs to the brain using the redox system provides derivatives of centrally acting amines in which a primary, secondary or tertiary amine function has been replaced with a dihydropyridine/pyridinium salt redox system. These brain-specific analogs of centrally acting amines have been recently described in International Patent Application No. PCT/US85/00236, filed Feb. 15, 1985 and published Sept. 12, 1985 under International Publication No. WO85/03937. The dihydropyridine analogs are characterized by the structural formula ##STR4## wherein D is the residue of a cent acting primary, secondary or tertiary amine, and --N-- is a radical of the formula ##STR5## wherein the dotted line in formula (a) indicates the presence of a double bond in either the 4 or 5 position of the dihydropyridine ring; the dotted line in formula (b) indicates the presence of a double bond in either the 2 or 3 position of the dihydroquinoline ring system; m is zero or one; n is zero, one or two; p is zero, one or two, provided that when p is one or two, each R in formula (b) can be located on either of the two fused rings; q is zero, one, or two, provided that when q is one or two, each R in formula (c) can be located on either of the two fused rings; and each R is independently selected from the group consisting of halo, C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 alkoxy, C.sub.2 -C.sub.8 alkoxycarbonyl, C.sub.2 -C.sub.8 alkanoyloxy, C.sub.1 -C.sub.7 haloalkyl, C.sub.1 -C.sub.7 alkylthio, C.sub.1 -C.sub.7 alkylsulfinyl, C.sub.1 -C.sub.7 alkylsulfonyl, --CH=NOR'" wherein R'" is H or C.sub.1 -C.sub.7 alkyl, and --CONR'R" wherein R' and R", which can be the same or different, are each H or C.sub.1 -C.sub.7 alkyl. These dihydropyridine analogs act as a delivery system for the corresponding biologically active quaternary compounds in vivo. Due to its lipophilic nature, the dihydropyridine analog will distribute throughout the body and has easy access to the brain through the blood-brain barrier. Oxidation in vivo will then provide the quaternary form, which will be "locked" preferentially in the brain. In contradistinction to the drug-carrier entities described in Bodor U.S. Pat. No 4,540,564 and related publications, however, there is no readily metabolically cleavable bond between drug and quaternary portions, and the active species delivered is not the original drug from which the dihydro analog was derived, but rather is the quaternary analog itself. Each of the major dihydropyridine .revreaction. pyridinium redox systems for brain-targeted drug delivery thus has its own unique characteristics but also has properties in common with the other approaches. Common to the various approaches is introduction of a dihydropyridine-type nucleus into the drug molecule, which renders the dihydropyridine-containing drug derivative substantially more lipophilic than the parent drug from which it is derived. The increased lipophilicity enables the derivative to readily penetrate biological membranes, including the blood-brain barrier. Also common to the various approaches is the fact that the "redox" nature of the dihydropyridine-type moiety means that the lipophilic dihydropyridine form is oxidizable in vivo to the hydrophilic, ionic pyridinium salt form, thus locking in the brain either the active drug or its quaternary precursor, depending on which approach is employed. The dihydropyridine pyridinium salt redox carrier and analog systems have achieved remarkable success in targeting drugs to the brain in laboratory tests. This success is, of course, due in part to the highly lipophilic nature of the dihydropyridine-containing derivatives, which allows brain penetration. At the same time, the increased lipophilicity makes it practically impossible to formulate aqueous solutions of these derivatives for injection; moreover, even when the dihydropyridines are dissolved in organic solvents such as dimethylsulfoxide, they have a propensity for precipitating out of solution upon injection, particularly at higher concentrations, and especially at the injection site or in the lungs. Indeed, even in the absence of noticeable crystallization, it has been found that the redox derivatives frequently display not only the desired concentration in the brain but undesired lung concentrations as well, so that while the brain to blood ratios are at appropriate high levels, the initial lung to brain levels are high as well. Still further, the dihydropyridine-containing derivatives suffer from stability problems, since even in the dry state they are very sensitive to oxidation as well as to water addition. These problems must be overcome so that the dihydropyridine .revreaction. pyridinium salt redox systems can be fully commercialized. Applicant's parent U.S. patent application Ser. No. 07/139,755, filed Dec. 30, 1987, incorporated by reference herein, relates to a method for stabilizing the reduced, dihydropyridine forms of dihydropyridine .revreaction. pyridinium salt redox systems for brain-targeted drug delivery by forming inclusion complexes of the dihydropyridine forms with HPCD. The redox inclusion complexes also provide a means for increasing the ratio of initial brain to lung concentrations, thus leading to decreased toxicity, and in selected instances provide improved water solubility as well. Formulation of a particular redox system for estradiol "in a water-soluble .beta.-hydroxycyclodextrin" is reported by Bodor and co-workers in Estes et al, "Use of a Chemical Redox System for Brain Enhanced Delivery of Estradiol Decreases Prostate Weight," in Biological Approaches to the Controlled Delivery of Drugs, ed. R. L. Juliano, Annals of the New York Academy of Sciences, Volume 507, 1987, 334-336. Applicant's parent U.S. patent application Ser. No. 07/174,945, filed Mar. 29, 1988, incorporated by reference herein, relates to a method for decreasing the incidence of precipitation of a lipophilic and/or water-labile drug (i.e. a drug which is insoluble or only sparingly soluble in water and/or which is unstable in water) occurring at or near the injection site and/or in the lungs or other organs following parenteral administration, said method comprising parenterally administering said drug in an aqueous solution containing from about 20% to about 50% hydroxypropyl-.beta.-cyclodextrin. SUMMARY AND OBJECTS OF THE INVENTION One object of the present invention is to provide a method for stabilizing the reduced, dihydropyridine form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery. Another object of the present invention is to provide a method for increasing the ratio of brain to lung concentrations at early time points resulting from administration of the reduced, dihydropyridine form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery. Yet another object of the present invention is to provide a method for improving the water solubility of the reduced, dihydropyridine form of selected dihydropyridine .revreaction. pyridinium salt redox systems for brain-targeted drug delivery. Another object of the present invention is to provide improved pharmaceutical formulations containing the reduced, dihydropyridine form of a dihydropyridine pyridinium salt redox system for brain-targeted drug delivery. The foregoing objects are achieved by means of novel inclusion complexes of cyclodextrin selected from the group consisting of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrins with the reduced, dihydropyridine form of the dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery. Thus, the present invention provides a novel method for stabilizing the reduced biooxidizable, blood-brain barrier penetrating lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery, said method comprising complexing said reduced form with cyclodextrin selected from the group consisting of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrin. The present invention further provides a novel method for improving the water-solubility of the reduced, biooxidizable, bloodbrain barrier penetrating lipoidal form of dihydropyridine .revreaction. pyridinium salt redox systems for brain-targeted drug delivery, said method comprising complexing said reduced form with cyclodextrin selected from the group consisting of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrin. The present invention still further provides a novel method for increasing the ratio of brain to lung concentrations of drug at early time points resulting from administration of the reduced, biooxidizable, blood-brain penetrating lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox system for brain-targeted drug delivery, said method comprising administering said reduced form as its inclusion complex with cyclodextrin selected from the group consisting of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrin. BRIEF DESCRIPTION OF THE DRAWINGS Other objects and advantages of the present invention will be apparent from the following detailed description and accompanying drawings, in which: FIG. 1 is a phase-solubility diagram illustrating the increase in solubility of an estradiol-CDS, 17.beta.-[(1-methyl-1,4-dihydro-3-pyridinyl)carbonyloxy]estra-1,3,5 (10)-trien-3-ol, hereafter referred to as E.sub.2 -CDS ( .circle. ), with increasing concentrations of hydroxypropyl-.beta.-cyclodextrin in water; FIG. 2 is a graph comparing the brain concentrations of the quaternary cation, 17.beta.-[(1-methyl-3-pyridinium)carbonyloxy]estra-1,3,5(10)-trien-3-ol, hereafter referred to as E.sub.2 Q.sup.+, in % dose per gram of brain tissue, following systemic administration to rats of either 15 mg/kg E.sub.2 -CDS in dimethylsulfoxide ( .circle. ) or 5 mg/kg E.sub.2 -CDS in aqueous hydroxypropyl-.beta.-cyclodextrin ( ), corrected for dose; FIGS. 3a and 3b are a pair of semi-logarithmic plots, FIG. 3a comparing the concentrations of E.sub.2 -CDS in lung tissue in ug per gram dose following systemic administration to rats of either 15 mg/kg E.sub.2 -CDS in dimethylsulfoxide ( .circle. ) or 5 mg/kg E.sub.2 -CDS inclusion complex with hydroxypropyl-.beta.-cyclodextrin (.DELTA.) in water, corrected for dose, and FIG. 3b comparing the lung concentrations of the quaternary cation, E.sub.2 Q.sup.+ or Quat, following the same E.sub.2 -CDS administration; FIG. 4 is a bar graph illustrating, at selected time points, the concentrations of the quaternary cation, E.sub.2 Q.sup.+ or Quat, in the brain in ng per gram dose, following systemic administration to rats of either 15 mg/kg E.sub.2 -CDS in dimethylsulfoxide (.quadrature.) or 5 mg/kg E.sub.2 -CDS inclusion complex with hydroxypropyl-.beta.-cyclodextrin ( ) in water, corrected for dose; and FIG. 5 is a plot of first-order rate constants as a function of ferricyanide ion concentration, illustrating the effect of added hydroxypropyl-.beta.-cyclodextrin (HPCD) on the rate of E.sub.2 -CDS oxidation. DETAILED DESCRIPTION OF THE INVENTION The term "lipoidal" as used herein is intended to designate a redox moiety which is lipid-soluble or lipophilic. The terms "redox carrier system" and "redox analog system" are intended to designate two different approaches to targeting drugs to the brain using a dihydropyridine .revreaction. pyridinium salt system; compounds representing either of these approaches are contemplated for complexation with cyclodextrin selected from the group consisting of hydroxypropyl, hydroxyethyl, glucosyl, maltosyl and maltotriosyl derivatives of .beta.- and .gamma.-cyclodextrin (especially hydroxypropyl-.beta.-cyclodextrin) and use in accord with the present invention. The redox carrier system provides for brain-targeted drug delivery by means of carrier-drugs, which in their reduced form, which is the form intended for administration, can be represented by the formula wherein [D] is a centrally acting drug species and [DHC] is the reduced, biooxidizable, blood-brain barrier penetrating, lipoidal form of a dihydropyridine .revreaction. pyridinium salt redox carrier. In their oxidized form, which is the form "locked" in the brain from which the active drug is ultimately released, the carrier-drugs can be represented by the formula wherein X.sup.- is the anion of a non-toxic pharmaceutically acceptable acid, [D] is a centrally acting drug species and [QC].sup.+ is the hydrophilic, ionic pyridinium salt form of a dihydropyridine .revreaction. pyridinium salt redox carrier. The redox carrier approach is discussed hereinabove in the section entitled "BACKGROUND OF THE INVENTION"; historically, the carrier system is the second type of redox system developed for delivering drugs to the brain. Various aspects of the redox carrier system have been described in detail in Bodor U.S. Pat. No. 4,479,932, issued Oct. 30, 1984; Bodor U.S. Pat. No. 4,540,564, issued Sept. 10, 1985; Bodor et al U.S. Pat. No 4,617,298, issued Oct. 14, 1986; UNIVERSITY OF FLORIDA's International Application No. PCT/US83/00725, published under International Publication No. W083/03968 on Nov. 24, 1983; Bodor U.S. Pat. No. 4,727,079, issued Feb. 23, 1988; Bodor U.S. Pat. No. 4,824,850, issued Apr. 25, 1989; Bodor U.S. Pat. No. 4,829,070, issued May 9, 1989; and related publications. All of said patents and the international publication are incorporated by reference herein in their entirety and relied upon. The redox analog system provides for brain-targeted drug delivery by means of new compounds containing a dihydropyridine .revreaction. pyridinium salt portion which, unlike the redox carrier, is not readily metabolically cleavable from the original drug molecule. One redox analog approach, which provides derivatives of centrally acting amines in which a primary, secondary or tertiary amine function has been replaced with a dihydropyridine .revreaction. pyridinium salt redox system, is discussed hereinabove in the section entitled "BACKGROUND OF THE INVENTION"; historically, this analog system is the third type of redox system developed for delivering drugs to the brain. Various aspects of this analog system are described in detail in UNIVERSITY OF FLORIDA's International Application No. PCT/US85/00236, published under International Publication No. WO85/03937 on Sept. 12, 1985, incorporated by reference herein in its entirety and relied upon. Another redox analog approach provides novel amino acids and peptides containing them which comprise a dihydropyridine .revreaction. pyridinium salt portion, the redox system being appended directly or via an alkylene bridge to the carbon atom adjacent to the carboxyl carbon. These amino acids and peptides are described in detail in copending Bodor patent application Ser. No. 07/035,648, filed Apr. 7, 1987, incorporated by reference herein in its entirety and relied upon. Briefly, the novel redox amino acids in the reduced form have the structural formula ##STR6## wherein Z is either a direct bond or C.sub.1 -C.sub.6 alkylene and can be attached to the heterocyclic ring via a ring carbon atom or via the ring nitrogen atom; R.sub.1 is C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 haloalkyl or C.sub.7 -C.sub.12 aralkyl when Z is attached to a ring carbon atom; R.sub.1 is a direct bond when Z is attached to the ring nitrogen atom; R.sub.2 and R.sub.3, which can be the same or different, are selected from the group consisting of hydrogen, halo, cyano, C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 alkoxy, C.sub.2 -C.sub.8 alkoxycarbonyl, C.sub.2 -C.sub.8 alkanoyloxy, C.sub.1 -C.sub.7 haloalkyl, C.sub.1 -C.sub.7 alkylthio, C.sub.1 -C.sub.7 alkylsulfinyl, C.sub.1 -C.sub.7 alkylsulfonyl, --CH=NOR'" wherein R'" is hydrogen or C.sub.1 -C.sub.7 alkyl, and --CONR'R" wherein R' and R", which can be the same or different, are each hydrogen or C.sub.1 -C.sub.7 alkyl; or one of R.sub.2 and R.sub.3 together with the adjacent ring carbon atom forms a benzene ring fused to the heterocyclic ring, which benzene ring may optionally bear one or two substituents, which can be the same or different, selected from the group consisting of hydroxy, protected hydroxy, halo, cyano, C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 alkoxy, C.sub.2 -C.sub.8 alkoxycarbonyl, C.sub.2 -C.sub.8 alkanoyloxy, C.sub.1 -C.sub.7 haloalkyl, C.sub.1 -C.sub.7 alkylthio, C.sub.1 -C.sub.7 alkylsulfinyl, C.sub.1 -C.sub.7 alkylsulfonyl, --CH=NOR'" wherein R'" is hydrogen or C.sub.1 -C.sub.7 alkyl, and --CONR'R" wherein R' and R", which can be the same or each hydrogen or C.sub.1 -C.sub.7 alkyl; R.sub.4 is different, are each hydrogen or C.sub.1 -C.sub.7 alkyl; R.sub.4 is hydrogen or a carboxyl protective group; R.sub.5 is hydrogen or an amino protective group; and the dotted lines indicate that the compound contains a 1,4- or 1,6-dihydropyridine, a 1,4- or 1,2-dihydroquinoline, or a 1,2-dihydroisoquinoline ring system. The new dihydropyridine amino acid analogs depicted above and the corresponding oxidized forms are useful in the preparation of novel redox peptides of the partial formulas: ##STR7## the new peptide analogs of partial structure (A) act as a delivery system for the corresponding quaternary salts of partial structure (B) in vivo; the quaternary derivatives, which also are chemical intermediates to the dihydro compounds, are pharmacologically active or convertible in vivo to pharmacologically active peptides, and are characterized by site-specific and sustained delivery to the brain when administered via the corresponding dihydropyridine form. Methods for the preparation of these analog amino acids and peptides utilize methods known in the art for introduction of the dihydropyridine .revreaction. pyridinium salt moiety or a precursor thereof, e.g. from the aforementioned International Publications Nos. WO83/03968 and WO85/03937, appropriately combined with well-known methods for peptide synthesis. Ultimately, the quaternary forms of the amino acids and peptides are subjected to reduction to afford the corresponding dihydropyridines, according to the methods of the Bodor U.S. patents and above-mentioned published PCT applications. In a preferred aspect of the present invention, the redox system selected for complexation with a hydroxypropyl, hydroxyethyl, glucosyl, maltosyl or maltotriosyl derivative of .beta.- or .gamma.-cyclodextrin and use in accord with the present invention is a redox carrier system. The drug and carrier portions of the redox carrier system are described in more detail below and of course in the various carrier patents and patent applications identified above and incorporated by reference herein. Selection of appropriate drugs and carrier moieties need not be limited to specific drugs and specific carriers disclosed in the aforementioned patents and applications or in the present application, just so long as the selected drug and carrier meet the general requirements of the drug/carrier system as described in the aforenoted documents. The term "drug" as used herein means any substance intended for use in the diagnosis, cure, mitigation, treatment or prevention of disease or in the enhancement of desirable physical or mental development and conditions in man or animal. By "centrally acting" drug species, active agent or compound as utilized herein, there is of course intended any drug species or the like, a significant (usually, principal) pharmacological activity of which is CNS and a result of direct action in the brain. Exemplary such centrally acting drug species are the CNS-amines and other nervous system agents, whether sympathetic or parasympathetic, e.g., phenylethylamine (a stimulant), dopamine (a neurotransmitter and dopaminergic agent used, e.g., in the treatment of Parkinsonism or hyperprolactinemia), tyramine (a stimulant), L-DOPA (a dopamine precursor used, for example, in the treatment of Parkinsonism); muscle relaxants, tranquilizers and antidepressants, e.g., benzodiazepine tranquilizers such as diazepam and oxazepam and phenothiazine tranquilizers such as carphenazine, fluphenazine and the like; mild and strong analgesics and narcotics; sedatives and hypnotics; narcotic antagonists; vascular agents; stimulants; anesthetics; small peptides, such as the di-, tri-, tetra and pentapeptides, and other small 2-20 amino acid unit containing peptides, e.g. the enkephalins (for example, Tyr-Gly-Gly-Phe-Leu), which, besides being analgesics, initiate epileptic activity in the brain at doses that are about tenfold lower than for effecting analgesic activity; growth-promoting substances; antiepileptic and anticonvulsant drugs generally, including hydantoins such as phenytoin and ethotoin, barbiturates such as phenobarbital; hormones, such as the steroid hormones, e.g., estradiol, testosterone, 17 .alpha.-ethynyl testosterone (ethisterone), and the like (recent studies on histological mapping of hormone-sensitive and specific steroid binding cells in the brain have underscored the importance of the steroid action in the brain on sexual behavior); amphetamine-like drugs; anticancer and anti-Parkinsonism agents; anti-hypertensives, agents to enhance learning capacity and the memory processes, including treatment of dementias, such as Alzheimer's disease, such as 9-amino-1,2,3,4-tetrahydroacridine; antibacterials; centrally acting hypotensive agents; centrally acting prostaglandins, such as PGD.sub.2 ; diagnostic agents, such as radiopharmaceuticals; monoamine oxidase (MAO) inhibitor drugs; CNS or brain important/essential amino acids, such as tryptophan (which is an antidepressant as well as a nutrient); and any like centrally acting compounds. For the purposes of this invention, dopa or L-DOPA is not classified as an amino acid but rather as a CNS amine and dopaminergic agent used, e.g. in the treatment of Parkinsonism. Other illustrative ultimate species of centrally acting drug entities are: amphetamine, dextroamphetamine, levamphetamine, aletamine, cypenamine, fencamfamin, fenozolone, zylofuramine, methamphetamine, phenmetrazine and phentermine, which are sympathomimetic amines/cerebral stimulants and appetite suppressants; etryptamine, a cerebral stimulant; codeine, oxycodone, pentazocine, anileridine, hydromorphone, morphine and oxymorphone, which are narcotic analgesics; desipramine, nortriptyline, octriptyline, maprotiline, opipramol and protriptyline, which are cerebral stimulants/tricylic antidepressants of the dibenzazepine type used, e.g., in endogenous depressions; clonidine and methyldopa, which are sympatholytic agents used, e.g., in hypertension; biperiden, cycrimine and procyclidine, which are centrally acting anticholinergics; tranylcypromine, a sympathomimetic cerebral stimulant/MAO inhibitor and antidepressant; acetophenazine, carphenazine, fluphenazine, perphenazine and piperacetazine, which are phenothiazine-type tranquilizers; benzoctamine, a sedative/muscle relaxant which structurally is an analogue of the phenothiazine tranquilizers; chlordiazepoxide, clorazepate, nitrazepam and temazepam, which are benzodiazepine-type tranquilizers; noracymethadol, a narcotic analgesic of the methadone type piminodine, a narcotic analgesic of the meperidine type; tracazolate, a sedative/hypotensive; prizidilol, a centrally acting hypotensive; sulpiride, an antidepressant/psychotropic; haloperidol and clopenthixol, which are tranquilizers; norepinephrine, a sympathetic stimulant/adrenergic agent; nalorphine and naloxone, narcotic antagonists; hydralazine, a hypotensive; ethotoin, phenobarbital and aminoglutethimide, anticonvulsants; epinephrine, an adrenergic agent; ethamivan, a medullary stimulant; bemegride, a barbiturate antagonist; amiphenazole, a stimulant; iopydol, iodopyracet, iodouppurate (o-iodohippuric acid), iodamide and iopanoic acid, which are radiodiagnostics; ephedrine, pseudoephedrine, oxymetazoline and phenylephrine, which are sympathomimetic amines and decongestants; estradiol, estrone and estriol, the natural estrogens; amoxicillin, oxacillin, carbenicillin, benzylpenicillin, phenoxymethylpenicillin, methicillin, nafcillin, ticarcillin, bacampicillin, epicillin, hetacillin, pivampacillin, the methoxymethyl ester of hetacillin, and ampicillin, which are penicillin-type antibiotics; amobarbital, a sedative; trihexyphenidyl, a centrally acting anticholinergic; hydroxyzine, a tranquilizer; chlortetracycline, demeclocycline, minocycline, doxycycline, oxytetracycline, tetracycline and methacycline, which are tetracycline-type antibiotics; flurazepam, bromazepam, demoxepam and lorazepam, benzodiazepine tranquilizers; phenytoin, an anticonvulsant; glutethimide, a mild hypnotic/sedative; clindamycin, lincomycin, nalidixic acid, oxolinic acid and phenazopyridine, antibacterials/antibiotics; bethanidine and guanethidine, hypotensives/sympatholytics; captopril, a hypotensive; methyprylon, a mild hypnotic; amedalin, bupropion, cartazolate, daledalin, difluanine, fluoxetine and nisoxetine, which are cerebral stimulants: propranolol, a .beta.-blocker antihypertensive; cloxacillin and dicloxacillin, penicillin-type antibacterials; butalbital, a barbiturate sedative; GABA, .gamma.-vinyl GABA, .gamma.-acetylenic GABA, neurotransmitters for possible use in epilepsy; valproic acid and its metabolites such as 5-hydroxy-2-n-propylpentanoic acid, 4-hydroxy-2-n-propylpentanoic acid, 3-hydroxy-2-n-propylpentanoic acid, for use as anticonvulsants; valpromide, a valproic acid derivative for use as an anticonvulsant; apomorphine, a narcotic depressant/emetic which has been used in the treatment of photosensitive epilepsy; pholcodine, a narcotic antitussive; methotrexate, mitoxantrone, podophyllotoxin derivatives (etopside, teniposide), doxorubicin, daunamycin and cyclophosphamide, anti-cancer/antitumor agents; methylphenidate, a stimulant; thiopental, an anesthetic; ethinyl estradiol and mestranol, estrogens; meptazinol, cyclazocine, phenazocine, profadol, metopon, drocode and myfadol, which are narcotic analgesics; buprenorphine, nalbuphine, butorphanol, levallorphan, naltrexone, nalmefene, alazocine, oxilorphan and nalmexone, which are narcotic antagonists or agonist-antagonists; norgestrel and norethindrone, progestins; cephalothin, cephalexin, cefazolin, cefoxitin, moxalactam, ceforanide, cefroxadine and cephapirin, cephalosporin antibiotics; atenolol, nadolol, timolol and metoprolol, .beta.-blockers/hypotensives; ACTH (corticotropin), a hormone which stimulates glucocorticoid production; LHRH, a neurotransmitter which stimulates secretion of the pituitary hormones, LH and FSH, and has been used to induce ovulation as well as for fertility control/contraception; sulfadiazine and other sulfonamide antibiotics; ribavirin and acyclovir, antiviral agents; chlorambucil and melphalan, nitrogen mustard-type anticancer/antitumor agents; methotrexate and aminopterin, which are folic acid antagonist-type anticancer/antitumor agents; platinum coordination complexes, i.e. cisplatin analogue-type anticancer/antitumor agents; dactinomycin and mitomycin C, used in cancer chemotherapy; thioguanine, a purine/pyrimidine antagonist used in cancer treatment; vincristine and vinblastine, anticancer alkaloids; hydroxyurea and DON, anticancer urea derivatives; FSH, HCG and HCS, pituitary and non-pituitary gonadotropins, used, for example, in certain reproductive disorders; N,N'-bis(dichloracetyl)-1,8-octamethylenediamine (fertilysin), an agent for male fertility inhibition; levorphanol, a narcotic analgesic; benzestrol and diethylstilbestrol, synthetic estrogens; ethyl .beta.-carboline-3-carboxylate, a benzodiazepine antagonist; furosemide, a diuretic/antihypertensive; dipyridamole and nifedipine, coronary vasodilators; and progabide, a GABA-agonist and prodrug of GABA. Yet other ultimate species include non-steroidal antiinflammatory agents/non-narcotic analgesics, e.g. propionic acid derivatives, acetic acid derivatives, fenamic acid derivatives and biphenylcarboxylic acid derivatives. Specific NSAID's/non-narcotic analgesics contemplated for use herein include ibuprofen, naproxen, flurbiprofen, zomepirac, sulindac, indomethacin, fenbufen, fenoprofen, indoproxen, ketoprofen, fluprofen, bucloxic acid, tolmetin, alclofenac, fenclozic acid, ibufenac, flufenisal, pirprofen, flufenamic acid, mefenamic acid, clonixeril, clonixin, meclofenamic acid, flunixin, diclofenac, carprofen, etodolac, fendosal, prodolic acid, sermetacin, indoxole, tetrydamine, diflunisal, naproxol, piroxicam, metazamide, flutiazin and tesicam. Preferred classes of centrally acting drugs for use herein are the central neurotransmitters, steroids, anticancer and antitumor agents, antiviral agents, tranquilizers, memory enhancers, hypotensives, sedatives, antipsychotics and cerebral stimulants (especially tricyclic antidepressants). Among the neurotransmitters, there can be mentioned amino acids, such as GABA, GABA derivatives and other omega-amino acids, as well as glycine, glutamic acid, tyrosine, aspartic acid and other natural amino acids; catecholamines, such as dopamine, norepinephrine and epinephrine; serotonin, histamine and tryptamine; and peptides such as neurotensin, luteinizing hormonereleasing hormone (LHRH), somatostatin, enkephalins such as met.sup.5 -enkephalin and leu.sup.5 -enkephalin, endorphins such as .gamma.-, .alpha.- and .beta.-endorphins, oxytocin M and vasopressin. Synthetic and semi-synthetic analogues, e.g. analogues of LHRH in which one or more amino acid(s) has/have been eliminated and/or replaced with one or more different amino acid(s), and which may be agonists or antagonists, are also contemplated, e.g. the primary and secondary amine LHRH analogues disclosed in U.S. Pat. Nos. 4,377,574, 3,917,825, 4,034,082 and 4,338,305. Among the steroids, there can be mentioned anti-inflammatory adrenal cortical steroids such as hydrocortisone, betamethasone, cortisone, dexamethasone, flumethasone, fluprednisolone, meprednisone, methyl prednisolone, prednisolone, prednisone, triamcinolone, cortodoxone, fludrocortisone, flurandrenolone acetonide (flurandrenolide), paramethasone and the like; male sex hormones (androgens), such as testosterone and its close analogues, e g methyl testosterone (17-methyltestosterone); and female sex hormones, both estrogens and progestins, e.g. progestins such as norgestrel, norethindrone, norethynodrel, ethisterone, dimethisterone, allylestrenol, cingestol, ethynerone, lynestrenol, norgesterone, norvinisterone, ethynodiol, oxogestone and tigestol, and estrogens such as ethinyl estradiol, mestranol, estradiol, estriol, estrone and e.g. quinestrol and the like. Among the anticancer and antitumor agents, there can be mentioned Ara-AC, pentostatin (2'-deoxycoformycin), Ara-C (cytarabine), 3-deazaguanine, dihydro-5-azacytidine, tiazofurin, sangivamycin, Ara-A (vitarabine), 6-MMPR, PCNU, FENU, HENU and other nitrosoureas, spiromustine, bisbenzimidazole, L-alanosine (6-diazo-5-oxo-L-norleucine), DON, L-ICRF, trimethyl TMM, 5-methyl-tetrahydrohomofolic acid, glyoxylic acid sulfonylhydrazone, DACH, SR-2555, SR-2508, desmethylmisonidazole, mitoxantrone, menogarol, aclacinomycin A, phyllanthoside, bactobolin, aphidocolin, homoharringtonine, levonantradol, acivicin, streptozotocin, hydroxyurea, chlorambucil, cyclophosphamide, uracil mustard, melphalan, 5-FU (5-fluorouracil), 5-FUDR (floxuridine), vincristine, vinblastine, cytosine arabinoside, 6-mercaptopurine, thioguanine, 5-azacytidine, methotrexate, adriamycin (doxorubicin), daunomycin (daunorubicin), largomycine polypeptide, aminopterin, dactinomycin, mitomycin C, and podophyllotoxin derivatives, such as etoposide (VP-16) and teniposide Among the antiviral agents, there can be mentioned ribavirin; acyclovir (ACV); amantadine (also of possible value as an anti-Parkinsonism agent); diarylamidines such as 5-amidino-2-(5-amidino-2-benzofuranyl)indole and 4',6-diimidazolino-2-phenylbenzo(b)thiophene; 2-aminooxazoles such as 2-guanidino-4,5-di-n-propyloxazole and 2-guanidino-4,5-diphenyloxazole benzimidazole analogues such as the syn and anti isomers of 6[[(hydroxyimino)phenyl]methyl] -1-[(1-methylethyl)sulfonyl]-1H-benzimidazol-2-amine; bridgehead C-nucleosides such as 5,7-dimethyl-2-.beta.-D-ribofuranosyl-s-triazole(1,5-a)pyrimidine; glycosides such as 2-deoxy-D-glucose, glucosamine, 2-deoxy-2-fluoro-D-mannose and 6-amino-6-deoxy-D-glucose; phenyl glucoside derivatives such as phenyl-6-chloro-6-deoxy-.beta.-D-glucopyranoside; (S)-9-(2,3-dihydroxypropyl)adenine; tiazofurin; selenazofurin; 3-deazauridine; 3-deazaguanosine; DHPG; 6-azauridine; idoxuridine; trifluridine (trifluorothymidine); BDVU (bisdihydroxyvinyluridine); zidovudine (AZT); dideoxycytidine; and 5,6-dichloro-1-.beta.-D-ribofuranosylbenzimidazole. Among the anticancer/antitumor and antiviral agents, those of the nucleoside type (i e a purine or pyrimidine base-type structure bearing a singly or multiply hydroxylated substituent) are of particular interest This group includes such compounds as Ara-AC, pentostatin, Ara-C, dihydro-5-azacytidine, tiazofurin, sangivamycin, Ara-A, 6-MMPR, desmethylmisonidazole, 5-FUDR, cytosine arabinoside, 5-azacytidine, ribavirin, acyclovir, (S)-9-(2,3-dihydroxypropyl)adenine, 6-azauridine, 5,6-dichloro-1-.beta.-D-ribofuranosylbenzimidazole, 5,7-dimethyl-2-.beta.-D-ribofuranosyl-s-triazole(1,5-a)pyrimidine, zidovudine (AZT), dideoxycytidine, dideoxyadenosine, dideoxyinosine and DHPG. Among the tranquilizers, there can be mentioned benzodiazepine tranquilizers, such as diazepam, oxazepam, lorazepam, chlordiazepoxide, flurazepam, bromazepam, chlorazepate, nitrazepam and temazepam; hydantoin-type tranquilizers/anticonvulsants such as phenytoin, ethotoin, mephenytoin; phenothiazine-type tranquilizers such as acetophenazine, carphenazine, fluphenazine, perphenazine and piperacetazine; and others. Among the hypotensives, there can be mentioned clonidine, methyldopa, bethanidine, debrisoquin, hydralazine, and guanethidine and its analogues. Among the sedatives, tranquilizers and antipsychotics, there can be mentioned the many specific compounds of this type disclosed above, especially the phenothiazines and benzodiazepines and their analogues. Among the cerebral stimulants, there also can be mentioned the many specific compounds set forth hereinabove, particularly the sympathomimetic amine-type cerebral stimulants and the tricyclic antidepressants, especially preferred tricyclics being the dibenzazepines and their analogues. Also illustrative of the centrally acting drug species contemplated by this invention are centrally active metabolites of centrally acting drugs. Such metabolites are typified by hydroxylated metabolites of tricyclic antidepressants, such as the E- and Z-isomers of 10-hydroxynortriptyline, 2-hydroxyimipramine, 2-hydroxydesipramine and 8-hydroxychloripramine; hydroxylated metabolites of phenothiazine tranquilizers, e.g. 7-hydroxychlorpromazine; and desmethyl metabolites of N-methyl benzodiazepine tranquilizers, e.g. desmethyldiazepam. Other CNS active metabolites for use herein will be apparent to those skilled in the art, e.g. SL 75102, which is an active metabolite of progabide, a GABA agonist, and hydroxy-CCNU, which is an active metabolite of CCNU, an anticancer nitrosourea Typically, these CNS active metabolites have been identified as such in the scientific literature but have not been administered as drugs themselves In many cases, the active metabolites are believed to be comparable in CNS activity to their parent drugs; frequently; however, the metabolites have not been administered per se because they are not themselves able to penetrate the blood-brain barrier. As indicated hereinabove, diagnostic agents, including radiopharmaceuticals, are encompassed by the expression "centrally acting drug" or the like as used herein. Any diagnostic agent which can be derivatized to afford a redox carrier system which will penetrate the BBB and concentrate in the brain in its quaternary form and can be detected therein is encompassed by this invention. The diagnostic may be "cold" and be detected by X-ray (e.g radiopaque agents) or other means such as mass spectrophotometry, NMR or other noninvasive techniques (e.g. when the compound includes stable isotopes such as C13, N15, O18, S33 and S34). The diagnostic alternatively may be "hot", i e radiolabelled, such as with radioactive iodine (I 123, I 125, I 131) and detected/imaged by radiation detection/imaging means. Typical "cold" diagnostics for derivation herein include o-iodohippuric acid, iothalamic acid, iopydol, iodamide and iopanoic acid. Typical radiolabelled diagnostics include diohippuric acid (I 125, I 131), diotyrosine (I 125, I 131), o-iodohippuric acid (I 131), iothalamic acid (I 125, I 131), thyroxine (I 125, I 131), iotyrosine (I 131) and iodometaraminol (I 123), which has the structural formula ##STR8## In the case of diagnostics, unlike the case of drugs which are for the treatment of disease, the "locked in" quaternary form will be the form that is imaged or otherwise detected, not the original diagnostic itself. Moreover, any of the centrally acting drugs which are intended for the treatment or prevention of medical disorders but which can be radiolabelled, e.g. with a radioisotope such as iodine, or labelled with a stable isotope, can thus be converted to a diagnostic for incorporation into the redox carrier system. It will be apparent from the known structures of the many drug species exemplified above, that in many cases the selected drug will possess more than one reactive functional group, and, in particular, that the drug may contain hydroxyl or carboxyl or amino or other functional groups in addition to the groups to which the carrier will be linked, and that these additional groups will at times benefit from being protected during synthesis and/or during administration. The nature of such protection is described in more detail in the various patents and patent applications incorporated by reference herein. Obviously, such protected drug species are encompassed by the definition of "drug" set forth hereinabove. It too will be appreciated that by "dihydropyridine carrier" or "[OHC]", there is intended any nontoxic carrier moiety comprising, containing or including the dihydropyridine nucleus, whether or not a part of any larger basic nucleus, and whether substituted or unsubstituted, the only criterion therefor being capacity for BBB penetration and in vivo oxidation thereof to the corresponding quaternary pyridinium salt carrier [QC].sup.+. As aforesaid, the ionic pyridinium salt drug/carrier prodrug entity [D-QC].sup.+ which results from such in vivo oxidation is prevented from efflux from the brain, while elimination from the general circulation is accelerated. Subsequently, the covalent or equivalent bond coupling the drug species [D] to the quaternary carrier [QC].sup.+ is metabolically cleaved, which results in sustained delivery of the drug [D] in the brain and facile elimination of the carrier moiety [QC].sup.+. Such "covalent or equivalent bond" between the drug and the quaternary carrier can be a simple direct chemical bond, e.g., an amide, an ester, or any other like bond, or same can even be comprised of a linking group or function, e.g. a thiazolidine bridge or a peptide linkage, typically necessitated when the drug species is not susceptible to direct chemical coupling to either the dihydropyridine carrier or the quaternary carrier. Nonetheless, the bond in the formulae [D-QC].sup.+ and [D-DHC] s intended to be, and is hereby defined as inclusive of all such alternatives. And the cleavage of the [D-QC] prodrug to sustainedly delivery the drug species [D] in the brain with concomitant facile elimination of the carrier moiety [QC].sup.+ is characteristically enzymatic cleavage, e.g., by esterase, amidase, cholinesterase, hydrolytic enzyme, or peptidase. The expression "non-toxic pharmaceutically acceptable salts" as used herein generally includes the nontoxic salts of the reduced, dihydropyridine forms of the redox carrier or redox analog systems, formed with nontoxic, pharmaceutically acceptable inorganic or organic acids HX. For example, the salts include those derived from inorganic acids such as hydrochloric, hydrobromic, sulfuric, sulfamic, phosphoric, nitric and the like; and the salts prepared from organic acids such as acetic, propionic, succinic, glycolic, stearic, lactic, malic, tartaric, citric, ascorbic, pamoic, maleic, hydroxymaleic, phenylacetic, glutamic, benzoic, salicylic, sulfanilic, fumaric, methanesulfonic, toluenesulfonic and the like. The expression "anion of a non-toxic pharmaceutically acceptable acid" as used herein, e.g. in connection with the oxidized, pyridinium salt forms of the redox carrier or redox analog systems, is intended to include anions of such inorganic or organic acids HX. In the discussion to follow, the expression "at least one reactive functional group selected from the group consisting of amino, hydroxyl, mercapto, carboxyl, amide and imide" or portions of that expression are used. The functional groups designated in that expression have the following meanings: The word "amino" means a primary or secondary H amino function, i.e. --NH.sub.2 or --NHR. The secondary amino function is also represented herein as --NH--, particularly since the exact identity of the R portion of -NHR is immaterial, R being a part of the drug residue D itself which is left unchanged by conversion of the drug to the redox carrier system. The word "hydroxyl" means an --OH function. The word "carboxyl" means a --COOH function. The word "mercapto" means an --SH function. The word "amide" means a carbamoyl (--CONH.sub.2) or substituted carbamoyl (--CONHR) or a sulfamoyl (--SO.sub.2 NH.sub.2) or substituted sulfamoyl (--SO.sub.2 NHR) functional group. The --CONHR and --SO.sub.2 NHR groups may also be represented herein as --CONH-- and --SO.sub.2 NH--, respectively, since the identity of R is immaterial, R being a part of the drug residue 0 itself which is left unchanged by conversion of the drug to the redox carrier system. The word "imide" means a functional group having the structure ##STR9## that is, the structure which characterizes imides (i.e. compounds having a succinimide-type or phthalimide-type structure). Many different dihydropyridine .revreaction. pyridinium salt redox carrier moieties are illustrated in the carrier patents and applications incorporated by reference hereinabove. The following is a list of representative major classes of dihydros and the corresponding quaternaries, but is not meant to be exhaustive: (1) For linkage to a drug having at least one hydroxyl or mercapto or primary or secondary amino functional grouping, replacing a hydrogen atom from at least one of said functional groupings with one of the following [DHC] groupings: ##STR10## wherein the dotted line in formulas (a'), (b') and (c') indicates the presence of a double bond in either the 4 or 5 position of the dihydropyridine ring; the dotted line in formulas (d'), (e') and (f') indicates the presence of a double bond in either the 2 or 3 position of the dihydroquinoline ring; R.sub.1 is C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 haloalkyl or C.sub.7 -C.sub.10 aralkyl; R.sub.3 is C.sub.1 to C.sub.3 alkylene; X is --CONR'R", wherein R' and R", which can be the same or different, are each H or C.sub.1 -C.sub.7 alkyl, or X is --CH=NOR'" wherein RD'" is H or C.sub.1 -C.sub.7 alkyl; the carbonyl-containing groupings in formulas (a') and (c') and the X substituent in formula (b') can each be attached at the 2, 3 or 4 position of the dihydropyridine ring; the carbonyl-containing groupings in formulas (d') and (f') and the X substituent in formula (e') can each be attached at the 2, 3 or 4 position of the dihydroquinoline ring; and the carbonyl-containing groupings in formulas (g') and (j') and the X substituent in formula (h') can each be attached at the 1, 3 or 4 position of the dihydroisoquinoline ring. (2) For linkage to a drug having at least one carboxyl functional groupings, replacing a hydrogen atom from at least one of said carboxyl groupings with one of the following [DHC] groupings: (a) When there are one or more --COOH groups to be derivatized: ##STR11## wherein the dotted line in formulas (i'), (ii') and (iii') indicates the presence of a double bond in either the 4 or 5 position of the dihydropyridine ring; the dotted line in formulas (iv'), (v') and (vi') indicates the presence of a double bond in either the 2 or 3 position of the dihydroquinoline ring; Z' is C.sub.1 -C.sub.8 straight or branched alkylene, preferably C.sub.1 -C.sub.3 straight or branched alkylene; Q is --O-- or --NH--; R.sub.1 is C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 haloalkyl or C.sub.7 -C.sub.10 aralkyl; R.sub.3 is C.sub.1 -C.sub.3 alkylene; X is --CONR'R" wherein R' and R", which can be the same or different, are each H or C.sub.1 -C.sub.7 alkyl, or X is --CH=NOR'" wherein R'" is H or C.sub.1 -C.sub.7 alkyl; the X substituent in formula (ii') and the carbonyl-containing grouping in formulas (i') and (iii') can each be attached at the 2, 3 or 4 position of the dihydropyridine ring; the X substituent in formula (v') and the carbonyl-containing groupings in formulas (iv') and (vi') can each be attached at the 2, 3 or 4 position of the dihydroquinoline ring; and the X substituent in formula (viii') and the carbonyl-containing groupings in formulas (vii') and (ix') can each be attached at the 1, 3 or 4 position of the dihydroquinoline ring; (b) Alternatively, when there is only one --COOH group to be derivatized: ##STR12## wherein the dotted line in formula (xii') indicates the presence of a double bond in either the 4 or 5 position of the dihydropyridine ring; the dotted line in formula (xiii') indicates the presence of a double bond in either the 2 or 3 position of the dihydroquinoline ring; is the skeleton of a sugar molecule; n.sup.iv is a positive integer equal to the total number of --OH functions in the sugar molecule from which said skeleton is derived; n.sup.v is a positive integer one less than the total number of --OH functions in the sugar molecule from which said skeleton is derived; each A in each of structures (xii'), (xiii') and (xiv') can independently be hydroxy or D', D' being the residue of a centrally acting drug containing one reactive carboxyl functional group, said residue being characterized by the absence of a hydrogen atom from said carboxyl functional group in said drug; and each R.sub.4 in each of structures (x') and (xi') can independently be hydroxy, ##STR13## wherein the dotted line is defined as with structures (xii') and (xiii'); D' is defined as with structures (xii'), (xiii') and (xiv') R.sub.1 is C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 haloalkyl or C.sub.7 -C.sub.10 aralkyl; and the depicted carbonyl groupings can be attached at the 2, 3 or 4 position of the pyridinium or quinolinium ring or at the 1, 3 or 4 at at least one R.sub.4 in each of structures (x') and (xi') is wherein R.sub.1, the dotted lines and the position of the carbonyl-containing groupings are defined as above; and with the further proviso that when more than one of the R.sub.4 radicals in a given compound are the aforesaid carbonyl-containing groupings, then all such carbonyl-containing groupings in said compound are identical. (3) For linkage to a drug having at least one --NH-- functional group which is part of an amide or imide structure or at least one low pKa primary or secondary amine functional group, replacing a hydrogen atom from at least one of said functional groupings with one of the following [DHC] groupings: ##STR14## wherein R is hydrogen, C.sub.1 -C.sub.7 alkyl, C.sub.3 -C.sub.8 cycloalkyl, C.sub.1 -C.sub.7 haloalkyl, furyl, phenyl, or phenyl substituted by one or more halo, lower alkyl, lower alkoxy, carbamoyl, lower alkoxycarbonyl, lower alkanoyloxy, lower haloalkyl, mono(lower alkyl)carbamoyl, di(lower alkyl)carbamoyl, lower alkylthio, lower alkylsulfinyl or lower alkylsulfonyl; the dotted line in formulas (k'), (l' ) and (m') indicates the presence of a double bond in either the 4 or 5 position of the dihydropyridine ring; the dotted line in formulas (n'), (o') and (p') indicates the presence of a double bond in either the 2 or 3 position of the dihydroquinoline ring; R.sub.1 is C.sub.1 -C.sub.7 alkyl, C.sub.1 -C.sub.7 haloalkyl or C.sub.7 -C.sub.10 aralkyl; R.sub.3 is C.sub.1 to C.sub.3 alkylene; X is --CONR'R", wherein R' and R", which can be the same or different, are each H or C.sub.1 -C.sub.7 alkyl, or X is --CH=NOR'" wherein R'" is H or C.sub.1 -C.sub.7 alkyl; the carbonyl-containing groupings in formulas (k') and (m') and the X substituent in formula (l' ) can each be attached at the 2, 3 or 4 position of the dihydropyridine ring; the carbonyl-containing groupings in formulas (n') and (p') and the X substituent in formula (o') can each be attached at the 2, 3 or 4 position of the dihydroquinoline ring; and the carbonyl-containing groupings in formulas (q') and (s') and the X substituent in formula (r') can each be attached at the 1, 3 or 4 position of the dihydroisoquinoline ring. Drugs containing secondary or tertiary hydroxyl functional groups can be linked to any of the [DHC] groupings (k') through (s') above in which the ##STR15## portion is derived from an aldehyde RCH.sub.2 O capable of reacting with said drug to form the corresponding hemiacetal, e.g. chloral, acetaldehyde, formaldehyde or benzaldehyde. The |