Fig. 1
Aspirin inhibition of the synthetic pathway of prostaglandins I2, E2, and thromboxane A2. Cyclooxygenases metabolize arachidonic acid to PGH2, which in turn is converted into various prostanoids by specific enzymes. Depending on the receptors activated by these molecules, mixed physiologic effects on the vasculature and platelet reactivity occur. Aspirin irreversibly inhibits cyclooxygenase activity. COXs = cyclooxygenases; PGH2 = prostaglandin H2; PGI synthase = prostaglandin-I synthase; PGE synthases = prostaglandin-E synthases; TXA synthase = thromboxane synthase; PGI2 = prostacyclin; PGE2 = prostaglandin E2; TXA2 = thromboxane A2; IP receptor = prostacyclin receptor; EP receptors = prostaglandin E2 receptors; TP receptors = thromboxane A2 receptors