RIGHT AND LEFT MYOCARDIAL ANTIOXIDANT RESPONSES DURING HEART-FAILURE SUBSEQUENT TO MYOCARDIAL-INFARCTION

Background Heart failure subsequent to myocardial infarction (MI) is a ccompanied by depressed antioxidants and increased oxidative stress in the myocardium. Antioxidant enzyme activities and oxidative stress we re examined in the viable left (LV) and right (RV) ventricles in relat ion to their hemodynamic function. Methods and Results The left corona ry artery in rats was ligated. At 1 week after MI, LV systolic pressur e (LVSP), LV end-diastolic pressure (LVEDP), and RV end-diastolic pres sure (RVEDP) remained near control values, whereas RV systolic pressur e (RVSP) was significantly elevated. In the 4, 8, and 16 week post-MI animals, LVSP was significantly reduced, with values of 112.0 +/- 1.57 , 99.9 +/- 0.52, and 89.2 +/- 1.4 mm Hg, whereas LVEDP was significant ly elevated, with values of 8.2 +/- 0.52, 17.4 +/- 1.7, and 31.4 +/- 1 .5 mmHg, respectively. RVEDP was higher at 8 and 16 weeks, and RVSP wa s significantly reduced at 16 weeks. At 1 week after MI, myocardial ca talase activity in the LV was maintained near control levels, whereas in the RV, it was 134% compared with its control value. At 4, 8, and 1 6 weeks, catalase activity in the LV was 71%, 48%, and 28% of respecti ve controls. Catalase activity in the RV was significantly reduced onl y at 16 weeks. A similar trend was seen-with respect to glutathione pe roxidase activity. Reduced/oxidized glutathione ratio was significantl y depressed in the LV at 1, 4, 8, and 16 weeks, whereas in the RV, thi s ratio was significantly reduced only at 8 and 16 weeks. Myocardial l ipid peroxidation in the LV at 4, 8, and 16 weeks was elevated by appr oximate to 40%, 51%, and 100%, respectively, whereas in the RV, an inc rease of approximate to 50% was seen only at 16 weeks. Conclusions The se data show that heart failure subsequent to MI is associated with an antioxidant deficit as well as increased oxidative stress, first in t he LV, followed by the RV. Furthermore, these changes correlated with the hemodynamic function in each of the ventricles, suggesting their r ole in the pathogenesis of ventricular dysfunction.