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Ann Thorac Surg 1996;61:1407-1411
© 1996 The Society of Thoracic Surgeons
National Heart & Lung Institute, Heart Science Centre, Harefield Hospital, Harefield, Middlesex, United Kingdom
Accepted for publication January 20, 1996.
Background. Heat-shock proteins are known to enhance cardiac resistance to ischemia.
Methods. To evaluate the kinetics of heat-shock protein 70 in relation to its effect on postischemic recovery of cardiac mechanical (cardiac output) and endothelial function (as percentage increase of coronary flow in response to 5-hydroxytryptamine), isolated rat hearts were subjected to prolonged hypothermic cardioplegic arrest at different intervals ranging from 12 to 96 hours after heat stress (n = 6 in each interval).
Results. Immunoblotting showed the maximal level of heat-shock protein 70, 0.65 ± 0.10 (arbitrary units ± standard error of the mean), at 24 hours after heat shock and similar values at 26 and 30 hours (p= not significant). Postischemic recovery of cardiac output and endothelial function (percentage of preischemic value ± standard error of the mean) observed at 24 hours was 74.0 ± 2.4 and 58.3 ± 7.2, respectively. Similar values were observed at 26 and 30 hours (p = not significant).
Conclusions. In a protocol mimicking conditions for cardiac transplantation, postischemic recovery of cardiac output and endothelial function was improved when the interval between heat stress and ischemia ranged from 24 to 30 hours. This correlated with an apparently critical amount of heat-shock protein 70.
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Ann. Thorac. Surg. 1996 61: 1411-1412.
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