Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury.
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 Ca(2+) 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 Ca(2+) handling. In conclusion, our results are consistent with the idea that chronic CO pollution dramatically increases the severity of myocardial I/R injuries.
Meyer
G
G
Research Laboratory: EA 4278, Physiology and Physiopathology of Cardiovascular Adaptations to Exercise, Faculty of Sciences, Avignon University, Avignon, France.
André
L
L
Tanguy
S
S
Boissiere
J
J
Farah
C
C
Lopez-Lauri
F
F
Gayrard
S
S
Richard
S
S
Boucher
F
F
Cazorla
O
O
Obert
P
P
Reboul
C
C
D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D000397:Air Pollution / Q000009:adverse effects*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D002118:Calcium / Q000502:physiology; D002248:Carbon Monoxide / Q000032:analysis / Q000633:toxicity*; D003331:Coronary Vessels / Q000502:physiology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006352:Heart Ventricles; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012518:Sarcomeres / Q000187:drug effects / Q000648:ultrastructure; D013482:Superoxide Dismutase / Q000378:metabolism
D000393:Air Pollutants; D000975:Antioxidants; D002248:Carbon Monoxide; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D002118:Calcium