期刊
CARDIOVASCULAR RESEARCH
卷 58, 期 3, 页码 575-581出版社
OXFORD UNIV PRESS
DOI: 10.1016/S0008-6363(03)00285-2
关键词
ventricular function; vasoconstriction/dilation; free radicals; preconditioning; hemodynamics
Objective: The purpose of this study was to determine whether exercise training could precondition the myocardium against hydrogen peroxide (H2O2)-induced damage. Methods: Male Fischer 344 rats ran on a treadmill for 9 weeks (60 min/day, 22 m/min, 6degrees grade, 5 days/week). Isolated perfused working hearts from exercise trained (ET, n=8) and sedentary (SED, n=10) animals were perfused with 150 muM H2O2. Results: Pre-H2O2 baseline values for cardiac external work (COxSP), coronary flow (CF), and lactate dehydrogenase (LDH) release were similar between groups. At 5 min of H2O2, COxSP was unchanged from baseline but CF was increased 30% in SED and 46% in ET (P<0.05 vs. SED). COxSP began to decline similarly thereafter in both groups, dropping to 20% of baseline at 20 min. CF in ET remained higher than SED throughout (P<0.05). LDH leakage remained near baseline during the first 15 min of H2O2 exposure, but was elevated (P<0.05) 72% in SED and 40% in ET after 20 min, and was 2.2-fold greater in SED than ET (P<0.05) after 25 min. Heat shock protein 70 was 2.1-fold greater in ET than SED (P<0.05), but ET did not change catalase and glutathione peroxidase. Conclusions: The results of this study indicate that chronic moderate exercise will enhance coronary flow and attenuate the development of myocardial injury when exposed to H2O2, but will not affect H2O2-induced decrease in pump function. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
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