THROMBIN GENERATION AS AN ACUTE EFFECT OF CIGARETTE-SMOKING

The effects of acute smoking on hemostatic functions were investigated in healthy young volunteers. Immediately after the volunteers smoked, a significant increase in blood pressure and heart rate was accompani ed by a rise in plasma epinephrine. Fibrinopeptide A and thrombin-anti thrombin III complex as markers of thrombin generation in vivo were si gnificantly increased after smoking. The increase in thrombin-antithro mbin III complex was significantly correlated with that of plasma epin ephrine. Both antigen and activity of tissue plasminogen activator and plasmin-inhibitor complex as markers of fibrinolytic activity in vivo were markedly increased after smoking, whereas D-dimer, plasminogen a ctivator inhibitor antigen, fibrinogen, and both beta-thromboglobulin and platelet factor 4 as markers of platelet activation in vivo were n ot changed. No effects were observed after sham smoking under exactly identical conditions in the same subjects. Thus thrombin generation wa s observed as acute hemostatic effects of smoking. Enhanced fibrinolyt ic response may counteract an increased procoagulant activity. Patient s with vascular disease might be more susceptible to a state of disequ ilibrium in favor of coagulation, which may partly explain a mechanism by which cigarette smoking leads to cardiovascular morbidity and mort ality.