IN-VITRO ANTIARRHYTHMIC EFFECT OF PRIOR WHOLE-BODY HYPERTHERMIA - IMPLICATION OF CATALASE

Citation
M. Joyeux et al., IN-VITRO ANTIARRHYTHMIC EFFECT OF PRIOR WHOLE-BODY HYPERTHERMIA - IMPLICATION OF CATALASE, Journal of Molecular and Cellular Cardiology, 29(12), 1997, pp. 3285-3292
Citations number
30
ISSN journal
00222828
Volume
29
Issue
12
Year of publication
1997
Pages
3285 - 3292
Database
ISI
SICI code
0022-2828(1997)29:12<3285:IAEOPW>2.0.ZU;2-M
Abstract
The protective effect of heat stress against mechanical dysfunction an d myocardial necrosis after prolonged ischemia is well known. We have investigated whether the protective effect of heat stress extends to r eperfusion arrhythmias in the isolated perfused rat heart. Rats were e xposed to 20 min of 42 degrees C hyperthermia. Twenty-four h later the ir hearts were isolated, perfused and subjected to a 5-min period of o cclusion of the left coronary artery. The incidence and duration of re perfusion arrhythmias were assessed in the 30-min reperfusion period. Prior heat stress led to a reduction in the incidence (from 100 to 60% , (P less than or equal to 0.05) and duration (from 611 +/- 251 to 62 +/- 51s, P less than or equal to 0.05) of ventricular tachycardia and/ or fibrillation, upon reperfusion following a 5-min ischemic period, T his prevention of reperfusion arrhythmias was associated with a two-fo ld increase in endogenous catalase activity and an enhanced heat stres s protein hsp 72 and 27 expression. Catalase inhibition by 3-amino tri azole (AT) abolished the antiarrhythmic effect of heat stress. The inc idence (80 v 100%) and duration (691 +/- 238 V 989 +/- 242 s) of reper fusion arrhythmias were not different between the group heat shocked AT and the group treated only with AT. On the other hand, in the pres ence of AT, myocardial noradrenaline release was attenuated by prior h eat stress upon stabilization: 3.9 +/- 0.8 compared to 9.4 +/- 2.1 pg/ ml/g tissue, P less than or equal to 0.05; upon reperfusion: 42.7+/-7. 3 compared to 69.8+/-9.5 pg/ml/g tissue, P less than or equal to 0.05) . In conclusion, heat stress leads to protection against reperfusion a rrhythmias occurring after a short ischemic insult, in the isolated ra t heart, Heat stress proteins and catalase seem to be implicated in th is protective effect. Finally, we have shown that in presence of AT, h eat stress decreases myocardial noradrenaline release. (C) 1997 Academ ic Press Limited.