Thromboxane A2, prostacyclin and aspirin: effects on vascular tone and platelet aggregation

Novel compounds that induce or inhibit platelet aggregation and constrict or dilate blood vessels were recently discovered. These compounds are all derivatives of arachidonic acid and include prostaglandin endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Thromboxane A2 (TxA2) could be one of the precipitating factors in coronary or cerebrovascular ischemia because it is a potent vasoconstrictor that is produced by platelets during their aggregation. On the other hand, prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation produced by vessel walls whose enhanced production should be beneficial. Aspirin inhibits prostaglandin endoperoxide synthetase and therefore prevents the subsequent production of TxA2, PGI2 and other prostaglandins. It has been suggested but not yet established that low doses of aspirin preferentially inhibit TxA2 biosynthesis. The roles of classic prostaglandins PGD2, PGE2 and PGF2 alpha in ischemia have not been determined.