Dipyridamole and other phosphodiesterase inhibitors act as antithrombotic agents by potentiating endogenous prostacyclin

Abstract

The antithrombotic effect of dipyridamole is through phosphodiesterase inhibition and depends on stimulation of platelet cyclic A.M.P. by circulating prostacyclin in the bloodstream. Low doses of aspirin selectively inhibit platelet cyclooxygenase and potentiate the antithrombotic effects of dipyridamole and theophylline. High doses of aspirin also prevent prostacyclin formation, thereby abolishing the effects of dipyridamole. Thus, the antithrombotic effectiveness of the combination of aspirin and dipyridamole depends critically on the doses used.