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Inhibition of Platelet Aggregation by Verapamil

1982; Lippincott Williams & Wilkins; Volume: 4; Issue: 2 Linguagem: Inglês

10.1097/00005344-198203000-00002

1533-4023

Lair G.T. Ribeiro, Tedd A. Brandon, Janet K. Horak, J. Anthony Ware, Richard R. Miller, R. Thomas Solis,

Acute Myocardial Infarction Research

Summary Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 ± 0.04 × 106/mm3, vs. control, 1.2 ± 0.09 × 106/mm3, (p > 0.05)). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 μM), was reduced by verapamil (verapamil, 15.3 ± 1.2 × 103 μm3 vs. control 24.4 ± 2.7 × 103 μm; p < 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 ± 1.1 × 103 μm3, vs. control, 17.3 ± 0.9 × 103 μm3 p < 0.001). We conclude that verapamil exerts an inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.