Inhibition of human platelet functions by cyclandelate.
The effects of cyclandelate and two of its metabolites, cyclandelate alcohol and acid, on several human platelet functions in vitro were investigated. Platelet aggregation was measured turbidimetrically using platelet-rich plasma. 14C-Serotonin (5-hydroxytryptamine) release from preloaded platelets, and thromboxane B2 (TxB2) formation were evaluated simultaneously with platelet aggregation. Cyclandelate and cyclandelate alcohol, but not cyclandelate acid, in a dose-dependent fashion prevented platelet aggregation and the concomitant 14C-serotonin release and TxB2 formation induced by adenosine diphosphate, platelet activating factor and collagen. In other experiments, inhibitory synergistic activities of cyclandelate and prostacyclin (PGI2) on platelet aggregation were demonstrated; cyclandelate alcohol and PGI2 showed a somewhat less pronounced synergism. The hypothesis that the calcium modulating property of cyclandelate is responsible for the inhibition of blood platelet functions is strengthened by the inability of the drug to inhibit the calcium-independent platelet aggregation induced by ristocetin.[1]References
- Inhibition of human platelet functions by cyclandelate. van den Hoven, W.E., Hall, D.W. Drugs (1987) [Pubmed]
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