Effect of heat shock precondition on reperfusion arrhythmia in rats / 中国病理生理杂志

ABSTRACT

AIM: To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS: Fifty-five Sprague Dawley rats were randomly divided into 2 groups the heat shock group (group H, n=29 ) and the control group (group C, n=26 ). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS: ①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na + channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION: Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na + channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.