Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest.
The aim of this study was to investigate the role of heat-shock proteins after heat-shock stress on the post-ischemic 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 degrees 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.
Amrani
M
M
Cardiothoracic Surgery Department, National Heart and Lung Institute, London, England.
Corbett
J
J
Allen
N J
NJ
O'Shea
J
J
Boateng
S Y
SY
May
A J
AJ
Dunn
M J
MJ
Yacoub
M H
MH
D000818:Animals; D002302:Cardiac Output; D006324:Heart Arrest, Induced; D006359:Heat Exhaustion / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats
D006360:Heat-Shock Proteins; D009569:Nitric Oxide