Effects of acute smoking on the hemostatic system in humans

Habitual smoking is one of the best established risk factors for cardiovascular disease. The pathogenesis of smoke‐induced damage is not so well clarified, but it probably includes—among some other aspects—an activation of the hemostatic system. Recently it has been shown that smoking a single cigarette can significantly decrease the coronary blood flow in coronary patients as well as in normal subjects. We tested the hypothesis that the acute effects of smoke are mediated by the hemostatic system. Seven healthy male volunteers, aged 20–40 years (mean 32±6 years), entered the study. All were habitual smokers, but had abstained from smoking in the 12 hours preceding the test. After lying in absolute rest for about 30 minutes, each subject smoked a cigarette containing 1.2 mg of nicotine. Immediately before and after smoking, blood was drawn by clear venipuncture for the evaluation of the following hemostatic variables: collagen‐induced platelet aggregation by the method of Born; thromboxane B2 (TxB2) production by platelets stimulated with collagen, radioimmunoassay (RIA); plasma beta thromboglobulin (TG) (RIA); plasma fibrinopeptide A (FPA) (RIA); plasma fibrinolytic activity in the euglobulin fraction (NEF) (fibrin plate method). The following results, respectively before and after smoking, were observed: collagen‐induced platelet aggregation 55±3 vs. 57±6%; TxB2 100.5±5.9 vs. 90.3±9.0 ng/108 platelets; plasma beta‐TG 20.8±2.2 vs. 19.2±2.3 ng/ml; plasma FPA 2.3±0.3 vs. 2.2±0.1 ng/ml; NEF, lysis diameter 16.8±1.6 vs. 16.7±1.7 mm; NEF + C1 inhibitor lysis diameter 8.8±0.7 vs. 9.1±0.7 mm. None of these variables was significantly changed after smoking. We conclude that acute smoking does not induce a prothrombotic state.