Kimura S, Nishinaga M, Ozawa T, Shimada K
Department of Cardiology, Jichi Medical School, Japan.
Am Heart J. 1994 Jul;128(1):7-11. doi: 10.1016/0002-8703(94)90003-5.
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 accompanied by a rise in plasma epinephrine. Fibrinopeptide A and thrombin-antithrombin III complex as markers of thrombin generation in vivo were significantly increased after smoking. The increase in thrombin-antithrombin III complex was significantly correlated with that of plasma epinephrine. 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 activator inhibitor antigen, fibrinogen, and both beta-thromboglobulin and platelet factor 4 as markers of platelet activation in vivo were not changed. No effects were observed after sham smoking under exactly identical conditions in the same subjects. Thus thrombin generation was observed as acute hemostatic effects of smoking. Enhanced fibrinolytic response may counteract an increased procoagulant activity. Patients with vascular disease might be more susceptible to a state of disequilibrium in favor of coagulation, which may partly explain a mechanism by which cigarette smoking leads to cardiovascular morbidity and mortality.
在健康年轻志愿者中研究了急性吸烟对止血功能的影响。志愿者吸烟后立即出现血压和心率显著升高，同时血浆肾上腺素水平上升。吸烟后，作为体内凝血酶生成标志物的纤维蛋白肽A和凝血酶 - 抗凝血酶III复合物显著增加。凝血酶 - 抗凝血酶III复合物的增加与血浆肾上腺素的增加显著相关。作为体内纤溶活性标志物的组织型纤溶酶原激活物和纤溶酶 - 抑制剂复合物的抗原和活性在吸烟后均显著增加，而作为体内血小板活化标志物的D - 二聚体、纤溶酶原激活物抑制剂抗原、纤维蛋白原以及β - 血小板球蛋白和血小板第4因子均未改变。在相同受试者的完全相同条件下进行假吸烟后未观察到任何影响。因此，观察到凝血酶生成是吸烟的急性止血效应。增强的纤溶反应可能抵消增加的促凝活性。血管疾病患者可能更容易出现有利于凝血的失衡状态，这可能部分解释了吸烟导致心血管发病和死亡的一种机制。
