EXCRETION OF THROMBOXANE METABOLITES IN HEALTHY WOMEN AFTER CESSATIONOF SMOKING

Cigarette smokers, but not former smokers, excrete more thromboxane A2 (TxA2) metabolites in the urine than do lifelong nonsmokers, which su ggests chronic activation of their platelets. To further characterize the effect elicited by smoking on platelet function, we followed the c hange in urinary excretion of the 2,3-dinor (Tx-M) and 11-dehydro (dTx ) metabolites of TxA2, analyzed by gas chromatography/mass spectrometr y and radioimmunoassay, respectively, in eight healthy women who quit habitual smoking and compared it with the recovery of these metabolite s after a single dose of acetylsalicylic acid (ASA). Tx-M and dTx befo re cessation of smoking were approximately 550 and 600 pg/mg creatinin e, respectively. Within 3 days after quitting smoking, Tx-M and dTx ha d dropped to stable levels of approximately 300 and 350 pg/mg, respect ively. The rates of change in excretion of Tx-M and dTx after smoking cessation were more rapid (p<0.02 and 0.02, respectively) than those o bserved during the recovery of platelet function after a single dose o f ASA. The excretion of 2,3-dinor-6-keto-prostaglandin F1alpha, a meta bolite of prostacyclin, was not affected by smoking cessation. We conc lude that cigarette smoking elicits an increase in platelet activity i n the absence of vascular injury. This increase is reversible within t he life span of the platelets.