The H l-receptor antagonist, bromadryl, was found to inhibit thrombin-stimulated aggregation, malondialdehyde formation and thromboxane B2 production in rat platelets [1]. This effect, observed under in vitro conditions, was dose-dependent and started at the concentration of 10 Ilmo1/1. Moreover, bromadryl administered orally to pregnant rats (in daily doses of 1 mg/kg for 18 days) significantly decreased ADP-stimulated platelet aggregation [2]. In the present study we investigated the effect of this drug on human platelets.

Bromadryl effectively inhibits thrombin-stimulated platelet aggregation in vitro, with a dose-dependent effect starting at 10 Ilmo1/1.

Paper

On the effect of the antihistaminic drug bromadryl on human platelets in vitro

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