Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury

Meyer G, Andre L, Tanguy S, Boissiere J, Farah C, Lopez-Lauri F, Gayrard S, Richard S, Boucher F, Cazorla O, Obert P, Reboul C. Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 298: H1445-H1453, 2010. First published March 5, 2010; doi:10.1152/ajpheart.01194.2009.-Myocardial damages due to ischemia-reperfusion (I/R) are recognized to be the result of a complex interplay between genetic and environmental factors. Epidemiological studies suggested that, among environmental factors, carbon monoxide ( CO) urban pollution can be linked to cardiac diseases and mortality. The aim of this work was to evaluate the impact of exposure to CO pollution on cardiac sensitivity to I/R. Regional myocardial I/R was performed on isolated perfused hearts from rats exposed for 4 wk to air enriched with CO (30-100 ppm). Functional variables, reperfusion ventricular arrhythmias (VA) and cellular damages ( infarct size, lactate dehydrogenase release) were assessed. Sarcomere length shortening and Ca2+ handling were evaluated in intact isolated cardiomyocytes during a cellular anoxia-reoxygenation protocol. The major results show that prolonged CO exposure worsens myocardial I/R injuries, resulting in increased severity of postischemic VA, impaired recovery of myocardial function, and increased infarct size (60 +/- 5 vs. 33 +/- 2% of ischemic zone). The aggravating effects of CO exposure on I/R could be explained by a reduced myocardial enzymatic antioxidant status (superoxide dismutase -45%; glutathione peroxidase -49%) associated with impaired intracellular Ca2+ handling. In conclusion, our results are consistent with the idea that chronic CO pollution dramatically increases the severity of myocardial I/R injuries.