Intermittent hypoxia exposure-induced heat-shock protein 70 expression increases resistance of rat heart to ischemic injury

AIM: To quantify the levels of HSP70 induced by different durations of inte rmittent thigh altitude) hypoxia and to correlate them with the degree of p rotection of the rat heart from ischemic injury. METHODS: Reverse transcrip tase polymerase chain reaction (RT-PCR) was used to detect the level of HSP 70 mRNA expression in rat myocardium. Ischemia/reperfusion injury was prese nted as severity of arrhythmias induced by occlusion and reperfusion of the left anterior descending coronary artery of rat heart. RESULTS: The level of HSP70 mRNA expression increased progressively along with the duration of intermittent hypoxia training. It was 2.6, 3.6, and 3.8 folds after 14-, 2 8-, and 42-d exposures compared to that of normoxia. The tolerance of rat h eart to ischemia/reperfusion injury increased with hypoxia pretreatment. Su ch an effect was significant after rat were exposed to a 28-d intermittent hypoxia (IH). The scores for ischemia and reperfusion inducing arrhythmia f or 28- and 42-d IH were 1.2 +/- 0.5, 1.0 +/- 0.5 and 1.0 +/- 0.5, 0.9 +/- 0 .5 (P < 0.01 compared with 4.0 +/- 0.7, 3.3 +/- 0.6 in normoxia rats). The overexpression of HSP70 and the increased tolerance to subsequent acute isc hemia/reperfusion injury could last for 2 wk after the rats (subjected to 2 8 d IH) returned to normoxia. Furthermore, there was a reverse correlation between the amount of HSP70 induced and the arrhythmia occurrence (r = -0.9 8, -0.92 for ischemia and reperfusion induced arrhythmia, P<0.01). CONCLUSI ON: These results suggest that increased resistance of rat heart to ischemi a/reperfusion injury after intermittent hypoxia exposure may be related to the amount of HSP70 induced.