Analysis of prostacyclin and thromboxane biosynthesis in cardiovascular disease.

THE APPRECIATION that two oxygenated metabolites 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 of to study platelet in

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