On the Mechanism of Platelet Function Inhibition by Acetylsalicylic Acid,

Abstract

Aspirin produces alteration of platelet function characterized by loss of secondary aggregation in response to ADP or epinephrine, and inhibition of aggregation by collagen. In addition, platelet factor 3 release by these reagents is reduced. A similar platelet lesion was produced by an acetylating agent, acetic anhydride, supporting earlier concepts that aspirin activity against platelets may be a consequence of acetylation. An attempt to identify specific acetylation of platelets with acetyl-1-14C salicylic acid was unsuccessful. Although platelet uptake of the label was demonstrated, metabolic incorporation of acetate could not be excluded.