Some Acute Effects of Smoking on Endothelial Cells and Platelets

Abstract

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.