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

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

› Institutsangaben

Abstract

als PDF herunterladen

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

PDF (705 kb)

Referenzen

References
1 Schafer AI, Handin RI. The role of platelets in thrombotic and vascular disease. Prog Cardiovasc Dis 1979; 22: 31-52
2 Weksler B, Gillick M, Pink J. Effect of propranolol on platelet function. Blood 1977; 49: 185-196
3 Schafer AI, Alexander BW, Handin RI. Inhibition of platelet function by organic nitrate vasodilators. Blood 1980; 55: 649-654
4 Han P, Genton E, Turpie AGG, Hirsh J, Gent M. Correlation between platelet survival, β-thromboglobulin and platelet aggregate ratio in patients with coronary artery disease. (Abstract) Circulation Part II 1978; 58: 116
5 Green LH, Seroppian E, Handin RI. Platelet activation during exercise-induced myocardial ischaemia. N Engl J Med 1980; 302: 193-197
6 Maseri A, L’Abbate A, Baroldi G. Coronary spasm as a possible cause of myocardial infarction: A conclusion derived from study of “preinfarction” angina. N Engl J Med 1978; 299: 1271-1277
7 Lewy RI, Smith JB, Silver MJ, Wiener L, Walinsky P. Detection of thromboxane B₂ in peripheral blood of patients with Prinzmetal’s angina. Prostaglandins and Medicine 1979; 2: 243-248
8 Mehta P, Mehta J. Platelet function studies in coronary heart disease: VIII. Decreased platelet sensitivity to prostacyclin in patients with myocardial ischaemia. Thromb Res 1980; 18: 273-277
9 Ikeda Y, Kikuchi M, Toyama K, Watanabe K, Ando Y. Inhibition of human platelet functions by verapamil. Thromb Haemostas 1981; 45: 158-161
10 Haeusler G. Differential effect of verapamil on exdtadon-contraction coupling in smooth muscle and on excitation-secretion coupling in adrenergic nerve terminals. J Pharmacol Exp Ther 1972; 180: 672-682
11 Nayler WG. The parmacology of disopyramide. J Int Med Res 1976; 4 (Suppl. 01) 8-12