Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

P Han; C Boatwright; N G Ardlie

doi:10.1055/s-0038-1657151

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1982; 47(02): 150-153
DOI: 10.1055/s-0038-1657151

Original Article

Schattauer GmbH Stuttgart

Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

Autor*innen

P Han

^*The School of Applied Science, Canberra College of Advanced Education, Canberra, ACT., Australia
C Boatwright

The Department of Medicine and Clinical Science, The John Curtin School of Medical Research, The Australian National University, Australia
N G Ardlie

The Department of Medicine and Clinical Science, The John Curtin School of Medical Research, The Australian National University, Australia

Abstract

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Summary

Various cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic add whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregation induced by the ionophore A23187.

Key words

Platelet inhibition - Verapamil - Disopyramide - Propranolol

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Referenzen

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