R.: Endogenous prostacyclin and thromboxane biosynthesis and platelet function during chronic administration of aspirin in

THE APPRECIATION that two oxygenated metabo-lites of arachidonic acid, prostacyclin (PGI2) and thromboxane A2 (TxA2), have potent and contrasting effects on vascular tone and platelet function in vitro has prompted attempts to define their importance in human vascular disease. Both compounds are formed from arachidonic acid by the enzyme cyclooxygenase via cyclic endoperoxide intermediates, PGG2 and PGH2. TxA2, the major cyclooxygenase product in the platelet, is a vasoconstrictor and potent stimulus to platelet aggregation in vitro. I PGJ2, a vasodilator and inhibitor of platelet aggregation, is the predominant product of the same enzyme in vascular endothelial cells.2 The development of techniques to study platelet function in vivo3 4 and ex vivo5 preceded the discover