Abstract

Blood platelets respond to the physiological agonist thrombin with shape change, aggregation and release of granular contents (1). Thrombin also evokes the rapid release of arachidonic acid esterified to platelet membrane phospholipids and thereby initiates the synthesis of prostaglandin endoperoxides, thromboxane A2 (TXA2) and other metabolites. The release of arachidonic acid from thrombin-stimulated platelets can be attributed largely to the action of PLA2 that specifically hydrolyzes phospholipids containing arachidonic acid (2,3). Platelet TXA2 generation represents a major pathway mediating both physiological and pathological platelet activities (4,5) and therefore the modulation of the involved PLA2 in platelets may play an important role in both haemostasis and thrombosis.

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