摘要
The primary objective of this article is to analyze the role of tobacco smoke compounds able to damage the cardiovascular system and, in particular, to interfere with blood pressure. They are products of tobacco plant leaves, like nicotine, thiocyanate and aromatic amines, and a chemical derived from cigarette com-bustion, carbon monoxide. Of the other thousands of chemicals, there is no clear evidence of cardiovascular damage. Nicotine and its major metabolite, cotinine, usually increase blood pressure by a direct action and an action stimulating neuro-humoral metabolites of the body as well as sympathetic stimulation. An indirect mechanism of damage exerted by elevated carboxyhe-moglobin concentrations is mediated by carbon mon-oxide, which, mainly induces arterial wall damage and, consequently, late rising in blood pressure by a toxic direct action on endothelial and blood cells. Thiocya-nate, in turn, reinforces the hypoxic effects determined by carbon monoxide. Aromatic amines, depending on their chemical structure, may exert toxic effects on the cardiovascular system although they have little effect on blood pressure. A rise in blood pressure determined by smoking compounds is a consequence of both their direct toxicity and the characteristics of their chemical chains that are strongly reactive with a large number of molecules for their spatial shape. In addition, a rise in blood pressure has been documented in individuals smoking a cigarette, acutely and chronically, with irre-versible artery wall alterations several years after begin-ning smoking. Since cigarette smoking has a worldwide diffusion, the evidence of this topic meets the interest of both the scientifc community and those individuals aiming to control smoking.
The primary objective of this article is to analyze the role of tobacco smoke compounds able to damage the cardiovascular system and, in particular, to interfere with blood pressure. They are products of tobacco plant leaves, like nicotine, thiocyanate and aromatic amines, and a chemical derived from cigarette combustion, carbon monoxide. Of the other thousands of chemicals, there is no clear evidence of cardiovascular damage. Nicotine and its major metabolite, cotinine, usually increase blood pressure by a direct action and an action stimulating neuro-humoral metabolites of the body as well as sympathetic stimulation. An indirect mechanism of damage exerted by elevated carboxyhemoglobin concentrations is mediated by carbon monoxide, which, mainly induces arterial wall damage and, consequently, late rising in blood pressure by a toxic direct action on endothelial and blood cells. Thiocyanate, in turn, reinforces the hypoxic effects determined by carbon monoxide. Aromatic amines, depending on their chemical structure, may exert toxic effects on the cardiovascular system although they have little effect on blood pressure. A rise in blood pressure determined by smoking compounds is a consequence of both their direct toxicity and the characteristics of their chemical chains that are strongly reactive with a large numberof molecules for their spatial shape. In addition, a rise in blood pressure has been documented in individuals smoking a cigarette, acutely and chronically, with irreversible artery wall alterations several years after beginning smoking. Since cigarette smoking has a worldwide diffusion, the evidence of this topic meets the interest of both the scientific community and those individuals aiming to control smoking.
