Hemodynamic and vascular effects of active and passive smoking.
Epidemiologic studies suggest that active and passive exposure to tobacco smoke is an important cause of cardiovascular morbidity and mortality. Numerous clinical studies have demonstrated that cigarette smoking causes coronary vasoconstriction, an increase in coronary vascular resistance, and a decrease in coronary blood flow, despite an increase in myocardial oxygen demand. Cigarette smoking also induces diffuse or segmental coronary artery spasm. In habitual smokers, smoking one cigarette increases heart rate, blood pressure, cardiac index, and myocardial oxygen demand and impairs cardiac performance, probably through adrenergic stimulation and catecholamine release. Several experimental studies, however, show that cigarette smoke inhalation causes pulmonary vasodilation because of inhalation of NO and CO in the vapor phase of cigarette smoke. Similar to active smoking, passive smoking has the same adverse effects on the cardiovascular system, with similar changes in hemodynamics and coronary vasomotor tone, platelet activation, impairment of endothelium-dependent vasodilation, and endothelial dysfunction. The adverse cardiovascular effects of smoking can be partially abolished by alpha- and beta-blockers or by calcium entry blockers.
D000818:Animals; D002320:Cardiovascular Physiological Phenomena; D006439:Hemodynamics; D006801:Humans; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology*; D014028:Tobacco Smoke Pollution; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D014666:Vasomotor System / Q000503:physiopathology*
D014028:Tobacco Smoke Pollution