Circulation, Vol 87, 963-971, Copyright © 1993 by American Heart Association
RW Currie, RM Tanguay and JG Kingma Jr
BACKGROUND. Induction of stress proteins, such as heat-shock protein 71
(HSP71), is associated with cardioprotection in isolated ischemic
myocardium. We tested this hypothesis in rabbits pretreated with whole-
body hyperthermia and then subjected to 30 or 45 minutes of regional
coronary occlusion (CO) followed by 3 hours reperfusion (Rep). METHODS AND
RESULTS. Control rabbits did not undergo whole-body hyperthermia;
heat-shocked (HS) rabbits were subjected to whole-body hyperthermia at 42
degrees C for 15 minutes. Rabbits were allowed to recover from whole- body
hyperthermia for 24 or 40 hours and were then subjected to CO/Rep. Heart
rate and arterial blood pressure were recorded during the experiments. Area
of necrosis (tetrazolium staining) was normalized to anatomic risk zone
size (microsphere autoradiography). In rabbits treated with whole-body
hyperthermia and 24 hours of recovery, infarct size was significantly
reduced in HS rabbits compared with control rabbits (41.2 +/- 7.8% versus
23.2 +/- 6.6%; p < or = 0.05; mean +/- SD) after 30 minutes of CO and 3
hours of Rep. Risk zone size was similar for the two experimental groups.
In rabbits treated with whole- body hyperthermia and 40 hours of recovery,
infarct size was similar for control and HS animals with either 30 or 45
minutes of CO (p = NS) and 3 hours of Rep. Risk zone size and area of
necrosis were similar for these experimental groups. Biopsies from ischemic
and nonischemic myocardium were obtained from rabbits at 24 and 40 hours
after heat shock and control rabbits to verify expression of HSP71;
expression was determined by Western blot analysis. CONCLUSIONS. Our
findings demonstrate a considerable increase in expression of HSP71 in
myocardium from hyperthermia-treated rabbits. Infarct size was
significantly reduced after 30 minutes of CO and 3 hours of Rep in hearts
at 24 but not 40 hours after heat shock compared with control hearts. We
conclude that heat shock-induced cardioprotection is transient and delays
the onset of irreversible myocardial injury caused by ischemia.
ARTICLES
Heat-shock response and limitation of tissue necrosis during occlusion/reperfusion in rabbit hearts
Department of Anatomy, Faculty of Medicine, Dalhousie University, Halifax.
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