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分离的肝细胞在器官保存液中4℃可保存6天,在恢复正常温度和正常氧量孵育时引起肝细胞活力丧失。为探讨低温所致肝细胞损伤的机制,观察了多种可致肝细胞损伤条件下,甘氨酸的保护作用。材料和方法:在含有3mmol/L甘氨酸或不含甘氨酸的肝细胞悬液中分别加入致损伤因素,37℃培养90分钟后测定乳酸脱氢酶的释放量和ATP浓度以评价肝细胞活力。结果:缺氧、线粒体抑制剂—氰化钾(3.Smmol/L)和碳酰氰m—氯苯腙(5,10μmol/L)均可引起肝细胞损伤:乳酸脱氢酶释出达60～90%,ATP
Isolated hepatocytes can be stored at 4 ° C for 6 days in organ preservation solution and cause loss of viability of hepatocytes upon recovery from normal temperature and incubation with normoxia. To investigate the mechanism of hypothermia induced hepatocellular injury, a variety of protective effects of glycine on hepatocyte injury were observed. MATERIALS AND METHODS: Injury factors were added into the suspension of hepatocytes containing 3mmol / L glycine or glycine without glycine, and the release of lactate dehydrogenase and the concentration of ATP were measured after 90 min incubation at 37 ℃ to evaluate the viability of hepatocytes. RESULTS: Hypoxia, mitochondrial inhibitor potassium cyanide (3.Smmol / L) and carbonyl cyanide m-chlorophenyl hydrazone (5,10μmol / L) all induced hepatocellular injury: lactate dehydrogenase reached 60 ~ 90%, ATP