Antioxidant and oxidative stress changes during heart failure subsequent to myocardial infarction in rats.
Antioxidant enzyme activities and oxidative stress were evaluated in the myocardium in relation to hemodynamic function subsequent to myocardial infarction in rats. One week after the coronary ligation, the left ventricular peak systolic pressure, left ventricular end-diastolic pressure, and aortic pressures remained near control values and there were no differences in lung and liver wet/dry weight ratios between experimental and control animals. In the 4-, 8-, and 16-week experimental animals, there was a progressive drop in left ventricular peak systolic pressure and an increase in left ventricular end-diastolic pressure. Aortic systolic pressure was depressed at 8 and 16 weeks. In myocardial infarct rats, there was a significant increase in wet/dry weight ratio of lungs at 8 weeks and at 16 weeks; this ratio was increased for lungs as well as liver. Based on the hemodynamic data as well as other observations, animals in the 1-, 4-, 8-, and 16-week groups were arbitrarily categorized into nonfailure and mild, moderate, and severe failure stages, respectively. In the nonfailure stage, there was a marginal increase in superoxide dismutase, glutathione peroxidase, and catalase activities as well as vitamin E levels. The redox state in these hearts, assessed by the reduced/oxidized glutathione ratio, was significantly increased. Superoxide dismutase activity was unchanged in mild and moderate failure stages but significantly depressed at 16 weeks. Glutathione peroxidase and catalase activities showed progressive decreases through mild, moderate, and severe failure stages. Vitamin E levels were significantly depressed at moderate and severe failure stages. There was a progressive increase in lipid peroxidation at mild, moderate, and severe stages of heart failure and the redox ratio was significantly depressed in the severe failure stage. These data suggest that heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress.
Department of Physiology, St. Boniface General Hospital Research Center, University of Manitoba, Winnipeg, Canada.
M F
MF
Hill
P K
PK
Singal
D000818:Animals; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006333:Heart Failure / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism*; D014810:Vitamin E / Q000378:metabolism
D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione