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Calcium antagonist activity of vinpocetine and vincamine in several models of cerebral ischaemia
Author(s) -
Lamar JeanClaude,
Poignet Hervé,
Beaughard Michèle,
Dureng Georges
Publication year - 1988
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430140322
Subject(s) - vinpocetine , flunarizine , nimodipine , pharmacology , diltiazem , chemistry , in vivo , calcium , antagonist , ischemia , cinnarizine , nifedipine , verapamil , agonist , anesthesia , medicine , biochemistry , receptor , biology , microbiology and biotechnology , organic chemistry
The potency and selectivity (i.e., the central vs. peripheral vascular smooth muscle activity) of the calcium antagonist (CA) effects of vinpocetine and vincamine have been compared with those of the standard CAs: flunarizine, verpamil, diltiazem, and nimodipine in rabbit basilar and splenic artery preparations. The cerebral antiischemic activity of these substances also was evaluated in five well‐documented in vivo models, i.e., hypobaric and normobaric hypoxia, global cerebral ischemia to MgCl 2 , cytotoxic anoxia with KCN, and cerebral edema induced by triethyl tin. Both vinpocetine and vincamine possess only weak CA activity, the potency order being: nimodipine > diltiazem > flunarizine = verapamil > vinpocetine > vincamine, with vinpocetine and flunarizine, in contrast to other compounds, showing a clear, 6‐ to 13‐fold selectivity for cerebral vascular smooth muscle. In the in vivo models, vinpocetine and flunarizine, together with vincamine, proved most active and had a larger spectrum of activity than the other CAs. These results suggest that the cerebrally selective CA effects of vinpocetine are at most only partly responsible for the effects of this compound in the in vivo models of cerebral ischemia.