The Role Of Heat Shock Protein27 In Intermittent Hypoxia Cardioprotection

The aim of this study was to investigate the cardiac protection afforded by intermittent hypoxia (IH) against ischemia/reperfusion (I/R) insult and its underlying mechanisms in rat heart. The main results are as follows:1, Isolated hearts from IH and control rats were subjected to 30 min global ischemia followed by 30 min reperfusion, recovery of cardiac function after ischemia was improved by IH. Cardiac myocytes isolated from IH and control rat hearts were exposed to 20 min simulated ischemia followed by 30 min reperfusion, increases in [Na+]i during I/R was significantly inhibited by IH, and the increase in [Ca +] was completely inhibited by IH.2, The improved cardiac function after I/R by IH was accompanied by an elevated preservation of the activity of p38. Pretreatment with SB, a specifc inhibitor of p38, abolished the effect of IH on HSP27 translocation during simulated I/R and resulted in decrease of contraction. Differential accumulation and location of HSP25 and B-crystallin in heart tissue during development imply distinct functions of both proteins, which seem to be involved in organization of cytoskeletal structures. As judged by level, phosphorylation state, and location of both small heat shock proteins, diseased adult human hearts share features with fetal hearts.3 , KATP antagonist glibenclamide eliminated the beneficial effects of IH on recovery of cardiac function after ischemia, but had no influence on control hearts. Simulated I/R induced an significant overload of [Na+]i and [Ca2+]i in control cardiac myocytes,but did not affect [Ca2+]i in IH cardiomytes. Glibenclamied and 5-HD, selective mitochondria! KATP antagonist respectively abolished this effect of IH; [Ca2+]i overload reappeared during I/R. Pinacidil, a KATP opener attenuated [Ca 2+]i overload during simulated I/R in control cardiac myoctes, but had no effect on[Ca2+]i change in IH myocytes.4. IH improved the recovery of cariac function after I/R inhibited [Na+] and [Ca2+] overload induced by simulated I/R. Better preservation of Na+/K+-ATPase, afciliated activation of KATP channel, p-HSP27 activation and translocation participated the cardioprotective effects afforded by IH.