Summary
It is suggested that passive smoking or smoke-exposure increase the risk of coronary heart disease. The same mechanisms as active smoking might play a role. The aim of this study was to determine whether exposure to smoke aggravated ischaemia/reperfusion injury. As a parameter of cellular function and integrity mitochondrial oxidative function was measured. Low molecular weight iron (LMWI) and α-tocopherol levels were determined to assess the possibility of toxic hydroxyl radical involvement in myocardial ischaemia/reperfusion injury of smoke-exposed rats. Rats were exposed to a small concentration of cigarette smoke for 2 months (the carboxyhemoglobin concentration did not increase), whereafter hearts were isolated and subjected to ischaemia and ischaemia followed by reperfusion. Mitochondrial oxidative function, low molecular weight iron and α-tocopherol were determined. The impairment in mitochondrial oxidative function, LMWI content elevation and the decrease in α-tocopherol concentration during ischaemia/reperfusion were significantly more severe in hearts of smoke-exposed rats than non-smokers. These results suggest that exposure to smoke increased the sensitivity of hearts to ischaemia/reperfusion injury, and that a free radical mechanism might participate.
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van Jaarsveld, H., Kuyl, J.M. & Alberts, D.W. Exposure of rats to low concentration of cigarette smoke increases myocardial sensitivity to ischaemia/reperfusion. Basic Res Cardiol 87, 393–399 (1992). https://doi.org/10.1007/BF00796524
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DOI: https://doi.org/10.1007/BF00796524