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Objective To study the cardioprotective effects of hypoxic preconditioning (HPC) on aged rat ventricular myocytes and the cellular mechanism of protection Methods In the model of hypoxia/reoxygenation (H/R) of isolated ventricular myocytes of aged rat, the effects of HPC on aged rat ventricular myocytes against lethal H/R stimulated ischemia/reperfusion (I/R) injury 24 hours later and the changes of mitogen activated protein kinase (MAPK) system were observed in the present study Results HPC attenuated the lactate dehydrogenase (LDH) release and ATP depletion in myocytes and increased the viability of myocytes It was also found that MAPK and its down stream kinase—S6 kinase were also activated after HPC Conclusion There is delayed cardioprotection in cardiac myocytes of aged rat and the cellular mechanism underlying might involve the activation of MAPK system
Objective To study the cardioprotective effects of hypoxic preconditioning (HPC) on aged rat ventricular myocytes and the cellular mechanism of protection Methods In the model of hypoxia / reoxygenation (H / R) of isolated ventricular myocytes of aged rat, the effects of HPC on aged rat ventricular myocytes against lethal H / R stimulated ischemia / reperfusion (I / R) injury 24 hours later and the changes of mitogen activated protein kinase (MAPK) system were observed in the present study Results HPC attenuated the lactate dehydrogenase (LDH) release and ATP depletion in myocytes and increased the viability of myocytes It was also found that MAPK and its down stream kinase-S6 kinase were also activated after HPC Conclusion There is delayed cardioprotection in cardiac myocytes of aged rat and the cellular mechanism underlying might involve the activation of MAPK system