IMPROVED TOLERANCE TO HYDROGEN PEROXIDE-INDUCED OXIDATIVE STRESS IN AGED RAT HEARTS





J.W. Starnes and R.P. Taylor

Department of Kinesiology
University of Texas
Austin, TX 78712




Reactive oxygen species, which includes hydrogen peroxide (H2O2), have been implicated in myocardial injury after ischemia-reperfusion injury and in the process of cardiac aging. The purpose of this study was to determine the effect of age on the ability of the heart to tolerate direct exposure of H2O2. Isolated perfused working hearts from 2.5-month, 8-month, and 23-month male F344 rats were perfused with H2O2-free buffer for approximately 25 minutes to establish a stable baseline function and then with 125 micomolar H2O2 for 20 minutes followed by a 10-minute washout with H2O2-free buffer. Pre-H2O2 baseline function (cardiac output x systolic pressure) was 4,197283 ml/min/g x mmHg at 2.5-mo (n, 4,455202 at 8-mo (, and 3,559159 at 23-mo (n . H2O2 exposure progressively decreased cardiac performance throughout the 20-minute period in all groups; however, the decline in the oldest group was significantly attenuated. After 20 minutes of exposure, cardiac function (% of pre-H2O2 baseline) was 22.23.5, 20.12.4, and 37.74.9 in the 2.5-, 8-, and 23-mo groups, respectively. Leakage of lactate dehydrogenase (LDH), a marker of tissue necrosis, was measured at 5-minute intervals throughout perfusion. LDH release during the 20-minute H2O2 exposure did not increase compared to baseline in the 2.5- or 23-mo groups, but was elevated 1.8-fold at 20 minutes in the 8-mo group (p<0.05). LDH release increased in all groups during the 10-minute washout period; however, the amount released by the oldest group was significantly less than the other groups and the amount released by the 8-mo group was significantly greater than the other groups. At the end of the perfusion, LDH release (mU/min/g) was 70.72.6, 142.211.5, and 35.75.4 in the 2.5-, 8-, and 23-mo groups, respectively (P<0.05 vs any group). The results of this study indicate that aged rat hearts can tolerate H2O2-induced oxidative stress better than hearts from younger animals. Supported Am. Heart Assoc., Texas Affiliate




Key words: ischemia-reperfusion, free radical, perfused heart, F344 rat







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