Abstract
The aim of this study was to investigate the role of heat-shock proteins after heat-shock stress on the postischemic recovery of cardiac mechanical and endothelial function following a prolonged cardiac arrest. Isolated working rat hearts were subjected to a cardioplegic arrest for 4 hours at 4 °C. Three groups (n = 8 in each) were studied: (1) control, (2) sham-treated, and (3) heat-shocked rats. Postischemic recovery of cardiac output and endothelial function (as percent of preischemic control values) was 57.8% ± 2.8% and 20.8% ± 3.9% in group 1, 50.9% ± 4.0% and 26.3% ± 5.9% in group 2, and 74.0% ± 2.4% and 51.2% ± 8.0% in group 3, respectively. Both postischemic myocardial and endothelial function were improved by heat stress.
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