Some acute effects of smoking on endothelial cells and platelets.
Some acute effects of smoking on endothelial cells and platelets.
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吸烟对内皮细胞和血小板的一些急性影响。
DOI：
10.1007/978-1-4684-5829-9_11
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发表时间：
1990
影响因子：
--
通讯作者：
James W. Davis
中科院分区：
文献类型：
--
作者：
James W. Davis
吸烟已被证实是动脉粥样硬化、闭塞性外周血管疾病和冠状动脉疾病的危险因素。2,3内皮损伤和血小板活化似乎是动脉粥样硬化和动脉血栓形成的重要机制。据报道，十多年前在五个不同的实验室使用三种不同的方法进行的研究表明，吸烟会急性增强血小板聚集。6-10随后，两份报告表明，吸烟对富血小板血浆中的血小板聚集没有急性影响，这些受试者在实验吸烟前没有说明戒烟的持续时间。11,12 Hladovec和Rossmann13描述了一种从血液中分离内皮细胞核残体的方法。这些细胞可能在脱离血管壁时失去了细胞核。We14显示，用荧光标记的抗因子VIII相关抗原抗体孵育后，尸体发出荧光，而同时孵育的皮肤切片没有显示上皮的荧光，倾向于证实从血液中分离的无核尸体的内皮起源。Prerovský和Hladovec15报道，志愿者吸两支烟后，内皮细胞的核死亡数量增加。Hladovec16描述了给药尼古丁后大鼠内皮细胞循环核尸体的增加，这表明这种化合物可能是吸烟诱导内皮细胞计数（ECC）增加的介质。在本章中，我将总结我们最近的一些工作，这些工作显示了主动和被动吸烟对不同人群的内皮细胞和血小板的急性影响。
Cigarette smoking is well established as a risk factor for atherosclerosis,1 occlusive peripheral vascular disease2 and coronary artery disease. 2,3 Endothelial damage and platelet activation appear to be among the more important mechanisms involved in the pathogenesis of atherosclerosis and arterial thrombosis. 4,5 Studies done more than a decade ago using three different methods in five different laboratories were reported to show acute enhancement of platelet aggregation by cigarette smoking. 6–10 Subsequently, two reports indicated no acute effect of cigarette smoking on platelet aggregation in the platelet-rich plasma of small groups of subjects whose duration of abstinence from tobacco before experimental smoking was not stated. 11,12 Hladovec and Rossmann13 described a method for the isolation of anuclear carcasses of endothelial cells from blood. The cells presumably lost their nuclei when they detached from vessel walls. We14 showed that the carcasses fluoresced after incubation with fluoresceinlabeled anti-factor VIII related antigen antibody, while simultaneously incubated sections of skin showed no fluorescence of the epithelium, tending to confirm an endothelial origin of the anuclear carcasses isolated from blood. Prerovský and Hladovec15 reported that counts of the anuclear carcasses of endothelial cells increased after volunteers smoked two cigarettes. Hladovec16 described an increase in circulating anuclear carcasses of endothelial cells in rats after administration of nicotine suggesting a potential role of this compound as a mediator of the smokinginduced increase in endothelial cell count (ECC). In this chapter I will summarize some of our recent work which shows acute effects of both active and passive smoking on the endothelium and platelets of various groups of subjects.