Objective: To investigate the protective effects of hypoxic preconditioning (HPC) on myocardial cells, and to determine the protective mechanism.
Methods: In the HPC model, the cells viability, productions of malondialdehyde (MDA), contents of ATP, lactate dehydrogenase (LDH), creatine kinase (CK), and expressions of intercellular adehesion molecule-1 (ICAM-1) were measured in the cultured myocardial cells of rats.
Results: HPC increased cells viability, attenuated the formation of lipid peroxides and ATP depletion, decreased the leakage of LDH and CK from the cells, and inhibited the increase of expression in intercellular adhesion molecule-1. The blocking agent of ATP sensitive K+ channel (K(ATP) channel), glibenclamide (Glb) completely abolished these protective effects of HPC.
Conclusion: The K(ATP) channel is an important effector of the protective effects of HPC, and the mechanism of the protective effects of HPC might be related to the inhibition of ICAM-1 expression.