<prompt> Low doses of aspirin prolong bleeding time by selec tively inhibiting synthesis of the following mediator in the plateletsThromboxane A25-HydroxytryptaminePlatelet activating factorProstacyclin  <response>: Antiplatelet aggregation:- Mech of action:- Aspirin inhibits COX irreversibly and thus inhibits synthesis of PGs. NSAIDs inhibit synthesis of both proaggregatory TXA2- synthesized in platelets and anti- aggregatory PGI2- synthesized by endothelium prostanoids, but effect on platelet TXA2 predominates . At therapeutic doses most NSAIDs inhibit platelet aggregation, bleeding time is prolonged. Therefore aspirin exes anti- thrombotic effect for several days. Risk of surgical and anticoagulant associated bleeding is enhanced. These drugs should be stopped a week before any elective major surgeries to reduce the risk of bleeding. Ref:- kd tripathi; pg num:-194 