Prostaglandins and platelet aggregation

Abstract

Prostaglandins may induce or inhibit platelet aggregation and constrict ro dilate blood vessels. Recent interest has focused on prostaglandins which are derivatives of arachidonic acid including prostaglandin, endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation whose enhanced production by vessel walls should be beneficial. It now appears that the circulating levels of PGI2 in man are extremely low and little is known about the manner in which to increase them. Furthermore, aspirin, in doses of as little as 4 mg/kg inhibits prostacyclin as well as thromboxane formation. Thromboxane A2 may be involved in coronary ischemia because it is a potent vasoconstrictor that is biosynthesized during platelet aggregation. Although thromboxane A2 is very unstable indirect evidence obtained by using thromboxane A generating systems or a stable analogue called carbocyclic thromboxane A2 (CTA2) suggests that it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow. The stable prostaglandins PGD2 and PGE2 are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2 inhibits platelet aggregation.