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Cigarette smoking is highly pathogenic to the vasculature. In smokers, the biosynthesis of both thromboxane (Tx) A2 and prostacyclin is increased. We hypothesized that the excess in prostacyclin biosynthesis in smokers was derived from the inducible cyclooxygenase-2 (COX-2). We further hypothesized that if the overproduction of prostacyclin in smokers were restraining platelet activation, then inhibition of COX-2 would lead to an increase in the activation of platelets, with a corresponding increase in the biosynthesis of TxA2.

Contribution of Cyclooxygenase-2 to Elevated Biosynthesis of Thromboxane A 2 and Prostacyclin in Cigarette Smokers

Contribution of Cyclooxygenase-2 to Elevated Biosynthesis of Thromboxane A ₂ and Prostacyclin in Cigarette Smokers