A STUDY ON LIVER INJURY CAUSED BY LIVER ISCHEMIA AND SEPTICEMIA

肝部分切除断流或连续阻断肝血管后肝损伤的实验研究：在正常大鼠和肝硬变大鼠中，总阻断时间为60min，比较了间歇阻断15min组(I组)、间歇阻断30min组(II组)和连续阻断60min组(III组)3种缺血方式对肝损伤的影响。I组细胞内钙离子浓度和肝酶活性最低。正常肝和肝硬变I组线粒体的ATP恢复、能荷恢复和磷化效率维持均令人满意。因此，在进行肝硬变切除术时，应采用15分钟的间歇性夹闭。另一方面，钙拮抗剂(盐酸维拉帕米)对大鼠缺血性肝损伤有保护作用。实验性内毒素血症大鼠肝细胞损伤及Calc…的保护作用更多的离子拮抗剂：连续静脉注射脂多糖造成大鼠实验性肝损伤，地尔硫卓与脂多糖同时注射(LD组)。用氯化Gd(GdC13)处理大鼠，观察Kupffer细胞在内毒素肝损伤中的作用。L组线粒体钙离子浓度升高，胞浆钙离子浓度升高。LD组大鼠心肌细胞胞浆和线粒体钙离子浓度明显降低。LD组大鼠血清肝酶升高和线粒体功能下降均受到明显抑制。L组和LD组大鼠血清嘌呤核苷磷酸化酶活性差异无统计学意义。另一方面，GdC13可显著抑制血清PNP活性和肝酶活性的升高。提示内毒素激活的Kupffer细胞损伤肝窦内皮细胞，肝细胞损伤加重。地尔硫卓通过抑制胞浆和线粒体中钙离子浓度的升高来保护实验性内毒素血症时的肝细胞。然而，地尔硫卓似乎并没有保护内皮细胞。较少

Experimental study of liver injury after partial hepatectomy with intermittent or continuous hepatic vascular occlusion : In normal and cirrhotic liver, rats, the total duration of clamping was 60 min and the liver damage following 3 ischemic modality were compared : a 15-min intermittent clamping group (Group I), a 30-min intermittent clamping group (Group II), and a 60-min continuous clamping group (Group III). The intracellular calcium concentration and hepatic enzyme were lowest in Group I.The recovery of ATP,energy charge and maintenance of phosphory lative efficiency of mitochondria was satisfactory in Group I,II in normal liver and Group I in cirrhotic liver. Therefore, when performing resection of a cirrhotic liver, a 15-min intermittent clamping should be adopted. On the other hand, calcium antagonist (Verapamil hydrochloride) revealed protective effect against ischemic liver injury.Liver cell damage induced by experimental endotoxemia in rats and protective effect of the calc … More ium antagonist : Experimental liver injury was induced by the continuous intravenous administration of lipopolys accharide (LPS,L-group) in rats, and diltiazem was also injected simultaneously with LPS (LD-group). The involvement of Kupffer cells in LPS induced liver injury was assessed in rats pretreated with Gadolinium chloride (GdC13). In the L-group, the level of calcium concentration in the mitochondria was elevated, then that in cytoplasm was elevated. The level of calcium concentration of cytoplasm and mitochondria was reduced significantly in the LD-group. The elevation of serum liver enzymes and decrease of mitochondrial function were significantly inhibited in the Ld-Group. There were no differences of serum purine nucleoside phosphorylase (PNP) activity between the L and LD groups. On the other hand, the elevation of serum PNP activity and liver enzymes were significantly inhibited by GdC13 pretreatment. These results suggest that the Kupffer cells, activated by LPS,injured sinusoidal endothelial cells, and the damage of hepatocytes progressed. Diltiazem protected the hepatocytes during experimental endotoxemia by inhibiting elevation of calcium concentration in the cytoplasm and mitochondria. Diltiazem did not, however, appear to protect the endothelial cells. Less