[Protective effects of hypoxic preconditioning on the hypoxic/reoxygenation injury of neonatal rats cardiomyocytes].
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.


CONCLUSIONS
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.
Chen
Ri
R
Cardiothoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China. chenri5424@si-na.com
Chen
Sheng-Xi
SX
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D015221:Potassium Channels; D018799:Intercellular Adhesion Molecule-1; D007770:L-Lactate Dehydrogenase