Myocardial oxidative stress changes during compensated rig t heart failure in rats

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Pichardo Velazquez, Julieta
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14-34% of heart failure cases are due to an impairment of the right ventricular function and nothing is known about oxidative stress changes in this condition. In order to address this problem, oxidative stress changes were examined in the right ventricle of rats administered monocrotaline (50 mg/Kg i.p.), a pyrrolizidine alkaloid known to produce pulmonary hypertension and right heart failure. Monocrotaline treatment resulted in reduced body weight gain and the treated animals were about 20% lighter than controls at 3 weeks post-treatment duration. These experimental animals showed signs of pulmonary distress manifested as shortness of breath, pallor and listlessness. In monocrotaline injected rats, right heart hypertrophy was confirmed by an almost 2 fold increase in ventricular weight. Both right ventricular systolic and end diastolic pressures were significantly increased, with a slight drop in heart rate. Lung as well as liver wet/dry weight ratios were unchanged in the monocrotaline group compared to the control. Myocardial antioxidant enzymes, catalase, glutathione peroxidase and superoxide dismutase in the right ventricle of monocrotaline treated rats were not different from the right ventricle of control animals. There were no differences with respect to the non-enzymatic antioxidant retinol. There was a significant decline in the vitamin E content of the right ventricle of the monocrotaline treated animals. Lipid hydroperoxide concentration in the right ventricle was three fold higher in the monocrotaline treated rats compared to the right ventricle of the control group. (Abstract shortened by UMI.)