Right and left myocardial antioxidant responses during heart failure subsequent to myocardial infarction

Heart failure subsequent to myocardial infarction (MI) is accompanied by depressed antioxidants and increased oxidative stress in the myocardium. Antioxidant enzyme activities and oxidative stress were examined in the viable left (LV) and right (RV) ventricles in relation to their hemodynamic function.

The left coronary artery in rats was ligated. At 1 week after MI, LV systolic pressure (LVSP), LV end-diastolic pressure (LVEDP), and RV end-diastolic pressure (RVEDP) remained near control values, whereas RV systolic pressure (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 significantly elevated, with values of 8.2+/-0.52, 17.4+/-1.7, and 31.4+/-1.5 mm Hg, respectively. RVEDP was higher at 8 and 16 weeks, and RVSP was significantly reduced at 16 weeks. At 1 week after MI, myocardial catalase 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 16 weeks, catalase activity in the LV was 71%, 48%, and 28% of respective controls. Catalase activity in the RV was significantly reduced only at 16 weeks. A similar trend was seen with respect to glutathione peroxidase activity. Reduced/oxidized glutathione ratio was significantly depressed in the LV at 1, 4, 8, and 16 weeks, whereas in the RV, this ratio was significantly reduced only at 8 and 16 weeks. Myocardial lipid peroxidation in the LV at 4, 8, and 16 weeks was elevated by approximately 40%, 51%, and 100%, respectively, whereas in the RV, an increase of approximately 50% was seen only at 16 weeks.

These data show that heart failure subsequent to MI is associated with an antioxidant deficit as well as increased oxidative stress, first in the LV, followed by the RV. Furthermore, these changes correlated with the hemodynamic function in each of the ventricles, suggesting their role in the pathogenesis of ventricular dysfunction.