Objective: To study the effects of hypoxic preconditioning (HPC) on cardioprotection and the mechanism of protection.Methods: In the model of hypoxic/reoxygenation (H/R) of cultured neonatal rat cardiomyocytes, the effects of HPC on neonatal rat cardiomyocytes against lethal H/R injury and the expression of intercellular adehesion molecule-1 (ICAM-1) were observed in the present study.Results: HPC attenuated the cellular damage of H/R, as shown by the increase of cell viability, attenuation of formation of lipid peroxides (MDA) and ATP depletion, lowering of the leakage of lactate dehydrogenase (LDH) and the creatine kinase (CK) from the cells, the blocking agent of ATP sensitive K+ channel (KAjp channel), glibenclamide (Gib), completely abolish these protective effects of HPC. H/R injury increase the expression in intercellular adehesion molecule-1. HPC inhibits the increase of expression in intercellular adehesion molecule-1. The results also show that Gib abolish the effect of HPC on the expression in intercellular adhesion molecule-1.Conclusion : HPC have protective effects on neonatal rat cardiomyocytes against lethal H/R injury. The KATP channel is an important effector of the protective effects of HPC, and the mechanism of the protective effects of HPC might involve the inhibition of ICAM-1 expression.
|