Exposure of rats to low concentration of cigarette smoke increases myocardial sensitivity to ischaemia/reperfusion


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.

DOI: 10.1007/BF00796524

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@article{Jaarsveld1992ExposureOR, title={Exposure of rats to low concentration of cigarette smoke increases myocardial sensitivity to ischaemia/reperfusion}, author={Hans van Jaarsveld and J. M. Kuyl and David W. Alberts}, journal={Basic Research in Cardiology}, year={1992}, volume={87}, pages={393-399} }