Oxygen Radicals and Tissue Damage in Heart Hypertrophy
Cyanide-resistant respiration in heart homogenates supplemented with 1 mM NADH was greater in hypertrophied homogenates (60 days banding) with respect to control homogenates, particularly when the homogenates were incubated in 100% oxygen. The intermyofibrillar mitochondria from hypertrophied hearts produced more superoxide radicals than subsarcolemmal mitochondria, and both values were greater than in the unbanded group. H202 formation was more evident in the intact mitochondria prepared from hypertrophied hearts than in those of the control hearts. Moreover, the perfusion of isolated hearts in anoxic and reox-ygenated conditions caused a greater lipoperoxidative and functional damage at the mitochondrial level in hypertrophied hearts than in the control hearts. These results, correlated with the reduction in mitochondrial function found in the overloaded hearts, suggest an involvement of the reactive species of oxygen in the formation of cardiac damage induced by prolonged aortic banding.
KeywordsAortic Stenosis Rabbit Heart Control Heart Hypertrophied Heart Cardiac Mitochondrion
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