Increase in endogenous antioxidant enzymes protects hearts against reperfusion injury.

Coarctation of the abdominal aorta in rats for 10 wk increased the heart weight-to-body weight ratio by 36% and peak left ventricular systolic pressure by 75%; there was no apparent change in the end-diastolic pressure, and animals did not show any clinical signs of heart failure. These hypertrophied (H) hearts showed increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) with no change in catalase. Lipid peroxide content as indicated by the malondialdehyde (MDA) level was lower in H hearts. There was no apparent difference in either Na+ and Ca2+ content or high-energy phosphates between sham (S) and H hearts. Control and H hearts were subjected to 10 min of ischemia (I) and 15 min of reperfusion (R). Contractile failure and rise in resting tension due to I, in both S and H hearts, were comparable. On reperfusion, H hearts showed better recovery of the developed force and resting tension as well as reduced incidence of arrhythmias when compared with corresponding S hearts. Both SOD and GSHPx activities were depressed due to I-R, but these activities were significantly higher in reperfused H hearts. Reperfused H hearts also showed a better maintenance of the ultrastructure and Na+ and Ca2+ contents, recovery of high-energy phosphates, and reduced MDA levels compared with S hearts. Supplementation of the perfusion medium with SOD (120 U/ml) and catalase (80 U/ml) significantly attenuated the I-R injury in S hearts, and the response in many ways was comparable to H hearts. The study documents the therapeutic potential of increased myocardial endogenous antioxidants against oxidative stress.