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pubmed-article:7589876pubmed:abstractTextTwo proposed mechanisms of diabetic neuropathy are microvascular ischaemia and a reduction in Na,K-ATPase activity. We evaluated the effect of cilostazol, a drug that is both a potent phosphodiesterase inhibitor that normalizes nerve Na,K-AT-Pase and a vasodilator, on nerve blood flow (NBF) to determine whether it would improve experimental diabetic neuropathy. We examined whether epineurally applied cilostazol acted as a vasodilator on the peripheral nerve of normal and diabetic rats, and whether feeding the rats a cilostazol-supplemented diet could improve diabetic neuropathy. Cilostazol increased nerve blood flow (NBF) in a dose-dependent fashion with an EC50 of 10(-5.74) mol/l. Cilostazol also normalized NBF in experimental diabetic neuropathy with a 10(-4) mol/l local application on the sciatic nerve. In diabetic neuropathy, a cilostazol-supplemented diet improved both NBF and nerve conduction in a dose- and time-dependent fashion. Potential mechanisms of action of cilostazol on the nerve include its effect on NBF, Na, K-ATPase, and restoration of the thromboxane:prostacyclin ratio. Cilostazol may have potential in the treatment of diabetic neuropathy.lld:pubmed
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pubmed-article:7589876pubmed:articleTitleEffect of cilostazol on experimental diabetic neuropathy in the rat.lld:pubmed
pubmed-article:7589876pubmed:affiliationDepartment of Neurology, Mayo Foundation, Rochester, Minnesota 55905, USA.lld:pubmed
pubmed-article:7589876pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7589876pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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