The Protective Effect of Heat Stress Against Reperfusion Arrhythmias in the Rat

Heat stress provides protection against mechanical dysfunction and myocardial necrosis after prolonged ischemia. We have investigated whether this protection extends to reperfusion arrhythmias occurring after a short (non-lethal) ischemic insult. Anaesthetized open chest rats were subjected to a 5-min occlusion of the left coronary artery. The incidence and duration of reperfusion arrhythmias and the duration of sinus rhythm were assessed in the first 5 min of reperfusion. Prior heat stress led to a reduction in the incidence (100-63%, P 0.05) and duration (66.2 ± 15.8 to 9.4 ± 2.9s, P 0.05) of ventricular tachycardia and a non-significant reduction in the incidence (76-50%) and duration (74.3 ± 23.4 to 42.9 ± 24.4s, P = 0.09) of ventricular fibrillation. This resulted in a significant increase in the duration of sinus rhythm (142.1 ± 27.6 to 216.7 ± 24.8s, P 0.05) and reduction in arrhythmia score (P 0.05) in heat stressed rats compared with controls. This protection against reperfusion arrhythmias was associated with a two-fold increase in endogenous catalase activity and expression of the inducible heat stress protein HSP 70. Inhibition of catalase with pre-administered 3-amino triazole resulted in a paradoxical protection in both sham and heat stress hearts. We conclude that heat stress leads to protection against reperfusion arrhythmias; however, we have been unable to resolve whether the changes in catalase activity of HSP expression are the mediators of the demonstrated cardioprotection.