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Ann Thorac Surg 1994;57:157-160
© 1994 The Society of Thoracic Surgeons

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Articles

Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest

Cardiothoracic Surgery Department, National Heart and Lung Institute, London, England

Accepted for publication March 4, 1993.

^_* Address reprint requests to Prof Yacoub, Cardiothoracic Surgery Department, National Heart and Lung Institute, Dovehouse St, London SW3 6LY, England.

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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