Acetylsalicylic acid irreversibly acetylates the enzyme cyclooxygenase found in platelets. This enzyme is necessary for the conversion of platelet arachidonic acid to throm-boxane A2. The latter is a powerful platelet-aggregating agent and vasoconstrictor. The conversion to thromboxane A2 and platelet aggregation can be initiated by several substances, especially those released following the inter¬action of catecholamine or platelets with subendothelial collagen. Endothelial and smooth muscle cells, when stimulated by physical or chemical injury, cause cyclooxy-genase to convert membrane arachidonic acid to prosta-cyclin which is then released. Prostacyclin is a powerful inhibitor of platelet aggregation as well as a potent vaso¬dilator. Aspirin reduces the formation of prostacyclin in the vessel wall and its undesirable effects. Low-dose aspirin inhibits thromboxane A2 synthesis and platelet aggrega¬tion, but does not appear to inhibit prostacyclin produc¬tion significantly.
Cyclooxygenase is also inhibited by all nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin transfers and acetyl group to the enzyme irreversibly inactivating the enzyme (see Fig. 2). Other NSAIDs such as ibuprofen, act as a reversible inhibitors of cyclooxygenase and thus cannot be depended on to cause sustained cardioprotection.

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