In vitro effects of gallopamil on platelet aggregation and thromboxane generation.

The in vitro effects of gallopamil, a highly specific calcium-channel blocker, on platelet function were investigated. Gallopamil caused a dose-dependent inhibition of platelet aggregation. In fact, the drug in concentrations as low as 0.5 microgram/ml inhibited platelet activating factor and epinephrine-induced platelet aggregation. Similarly, the inhibition of adenosine diphosphate and epinephrine-induced thromboxane generation was demonstrated. Since platelet activation and thromboxane release may be related to myocardial ischemia, it is conceivable that some of the antianginal effects of gallopamil may in part be due to platelet inhibitory effects.