摘要(Abstract)：

<正> The delayed cardicprotection of ischemic preconditioning(IPC)has beendemonstrated in heart in vivo and myocytes in vitro in different animal species.However,the cellular mechanism underlying delayed protection of IPC are not fullyunderstood at present.In the model of hypoxia/reoxygenation(H/R)of isolatedventricular myocytes of aged rat,effects of bypoxic preconditiong(HPC)onaged rat ventricular myocytes against lethal H/R simulated ischemia/reperfusion(I/R)injury 24 hours late and the changes of mitogen-activated protein kinase(MAPK)system were observed in the present study.The results showed that HPC attemuatedthe LDH release(72.9±11.4 vs 268.3±29.5,p<0.01)and ATP depletion(19.8±3.4vs 12,2±2.2,p<0.01)in myocytes and increased the visbility(66.0±4.0 vs 52.0±6.0,p<0.05).HPC induced activation of MAPK in myocytes at 5 min up to highpeak(83.2±10.1 vs control 11.0±1.8 pmol/min,mg pr~(-1),p<0.01),The MAPKactivity of aged myocytes were lower than that of neonatal myocytes and had astatistical significance(p<0.05).At 30 min after HPC.the MAPK activity of agedand neonatal rat myocytes were still at high level,and retumed to basic levels at 1h,then maintained to 24 h at that level.preincubation of the myocytes with PD_(098059)prevented the activation of MAPK both in aged end neonatal myocytes(p<0.01).The activation of S6 kinase-the down-stream kinase of MAPK was also observedafter HPC.The results suggest that there is delayed cardioprotection in aged ratcardiac myocytes and the cellular mechanism umderlying might involved theactivation of MAPK system.

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