Reduced myocardial injury due to exogenous oxidants in pressure induced heart hypertrophy.

Changes in myocardial function, structure, high energy phosphates and lipid peroxide content were examined in hypertrophied hearts exposed to partially reduced forms of oxygen (PRFO) in an ex vivo system. Heart hypertrophy in rats was produced by narrowing of the abdominal aorta for 6, 12, 24, and 48 weeks. During this period, a stable hypertrophy and hyperfunction with no clinical signs of heart failure is reported to be accompanied by an increase in myocardial superoxide dismutase and glutathione peroxidase activities and a decrease in lipid peroxide content (Gupta and Singal, Circ. Res. 64:398-406, 1989). A 10-min perfusion of sham control hearts with PRFO caused a significant decline in the developed force, +/- dF/dt and a rise in resting tension. These changes due to PRFO were significantly less in all groups of hypertrophied hearts. PRFO produced 80.8 +/- 4.2% increase in malondialdehyde (MDA) content in sham controls, while different groups of hypertrophied hearts showed significantly lesser increase (range 45-50%) in MDA. PRFO resulted in loss of myocardial ATP and CP in control and hypertrophied groups, but this loss was significantly less in all groups of hypertrophied hearts. Both quantitative and qualitative ultrastructural changes due to PRFO were also found to be less in hypertrophied hearts. There were no significant differences among 6- to 48-week hypertrophy groups in their response to PRFO. The study suggests that endogenous antioxidants may serve as putative stabilizers of myocardial subcellular as well as contractile functions against oxidative stress.