An enzymatic mechanism for the antithrombotic and antihemostatic actions of aspirin

Abstract

Aspirin-type drugs may inhibit irreversible clumping of human blood platelets by blocking the enzymatic conversion of arachidonic acid to a hitherto undiscovered factor, labile aggregation-stimulating substance, which triggers aggregation and to prostaglandin E(2), which sensitizes the platelets to its aggregatory effects.