Background The classic glycine receptor (GlyR) in the central nervous system is a ligand-gated membrane-spanningion channel.Recent studies have provided evidence for the existence of GlyR in endothelial cells,renal proximal tubularcells and most leukocytes.In contrast,no evidence for GlyR in myocardial cells has been found so far.Our recentresearches have showed that glycine could protect myocardial cells from the damage induced by lipopolysaccharide(LPS).Further studies suggest that myocardial cells could contain GlyR or binding site of glycine.Methods In isolated rat heart damaged by LPS,the myocardial monophasic action potential (MAP),the heart rate (HR),the myocardial tension and the activities of lactate dehydrogenase (LDH) from the coronary effluent were determined.The concentration of intracellular free calcium ([Ca~(2~+)]_i) was measured in cardiomyocytes injured by LPS and byhypoxia/reoxygenation (H/R),which excludes the possibility that reduced calcium influx because of LPS neutralized byglycine.Immunohistochemistry was used to detect the GlyR in myocardial tissue.GlyR and its subunit in the purifiedcultured cardiomyocytes were identified by Western blotting.Results Although significant improvement in the MAP/MAPD_(20),HR,and reduction in LDH release were observed inglycine+LPS hearts,myocardial tension did not recover.Further studies demonstrated that glycine could prevent ratmycordial cells from LPS and hypoxia/reoxygenation injury (no endotoxin) by attenuating calcium influx.Immunohistochemistry exhibited a positive green-fluorescence signaling along the cardiac muscle fibers.Westernblotting shows that the purified cultured cardiomyocytes express GlyR β subunit,but GlyR al subunit could not bedetected.Conclusions The results suggest that glycine receptor is expressed in cardiomyocytes and participates incytoprotection from LPS and hypoxia/reoxygenation injury.Glycine could directly activate GlyR on the cardiomyocytesand prevent calcium influx into the cardiomyocytes. Background The classic glycine receptor (GlyR) in the central nervous system is a ligand-gated membrane-spanningion channel. Published studies have provided evidence for the existence of GlyR in endothelial cells, renal proximal tubular cells and most leukocytes. In contrast, no evidence for GlyR in myocardial cells has been found so far. Our recentresearches have showed that glycine could protect myocardial cells from the damage induced by lipopolysaccharide (LPS) .Further studies suggest that myocardial cells could contain GlyR or binding site of glycine. Methods In isolated rat heart damaged by LPS, the myocardial monophasic action potential (MAP), the heart rate (HR), the myocardial tension and the activities of lactate dehydrogenase (LDH) from the coronary effluent were determined. The concentration of intracellular free calcium ([Ca ~ 2 ~ +)] _i) was measured in cardiomyocytes injured by LPS and by hypoxia / reoxygenation (H / R), which excludes the possibility that reduced calcium influx because of LPS n eutralized by glycine. Immunohistochemistry was used to detect the GlyR in myocardial tissue. GlyR and its subunit in the purified culture cardiomyocytes were identified by Western blotting. Results Although significant improvement in the MAP / MAPD - (20), HR, and reduction in LDH release were observed Inhibition studies of that glycine could prevent rat mycordial cells from LPS and hypoxia / reoxygenation injury (no endotoxin) by attenuating calcium influx. Immunohistochemistry FIGS. a positive green-fluorescence signaling along the cardiac muscle fibers. Westernblotting shows that the purified cultured cardiomyocytes express GlyR beta subunit, but GlyR al subunit could not bedetected. Conclusions The results suggest that glycine receptor is expressed in cardiomyocytes and participates incytoprotection from LPS and hypoxia / reoxygenation injury. Glycine could directly activate GlyR on the cardiomyocytes and prevent calcium influx into thecardiomyocytes.