Low dose aspirin inhibits platelet aggregation

For platelets aggregation two factors are very important. Platelets produce TXA2 (Thromboxane) which is having platelets aggregating effects.Endothelium produces PGI2 (Prostacyclin) - which is having  anti-aggregating  effect. COX is responsible for synthesis of TXA2 and PGI2 both. Mature platelet only express COX-1. They do not synthesize Fresh COX-1. In platelets, the major cyclooxygenase product is TxA2 (thromboxane A2).

A Labile inducer of platelet aggregation and a potent vasoconstrictor. Aspirin blocks production of TxA2 by acetylating cyclooxygenase-1 (COX-1). Because platelets do not synthesize new proteins, the action of aspirin on platelet COX-1 is permanent, lasting for the life of the platelet (7-10 days). Thus, repeated doses of aspirin produce a cumulative effect on platelet function. At lower doses of aspirin only function of platelet is affected as they can not…