A STUDY ON LIVER INJURY CAUSED BY LIVER ISCHEMIA AND SEPTICEMIA

断续或持续肝血管闭塞对肝部分切除术后肝损伤的实验研究：比较正常肝和肝硬化大鼠钳夹总时间为60 min和3种缺血模式下肝损伤情况：15 min间歇钳夹组（I组）、30 min间歇钳夹组（II组）和60 min连续钳夹组（III组）。ⅰ组细胞内钙浓度和肝酶最低，ⅰ组、ⅱ组正常肝脏和ⅰ组肝硬化肝脏线粒体ATP的恢复、能量电荷的恢复和磷酸化相对效率的维持均令人满意。因此，在进行肝硬化肝切除术时，应采用15分钟间歇夹持。钙拮抗剂盐酸维拉帕米显示出对缺血性肝损伤的保护作用。实验性内毒素血症对大鼠肝细胞的损伤及钙离子拮抗剂的保护作用：通过持续静脉注射脂多糖（LPS， l组）诱导大鼠实验性肝损伤，并同时注射地尔硫卓（ld组）。用氯化钆（GdC13）预处理大鼠，评估库普弗细胞在LPS诱导的肝损伤中的作用。l组先升高线粒体钙浓度，后升高细胞质钙浓度。ld组大鼠细胞质和线粒体钙浓度水平明显降低。ld组大鼠血清肝酶升高和线粒体功能下降明显受到抑制。血清嘌呤核苷磷酸化酶（PNP）活性在L组和LD组之间无显著差异。另一方面，GdC13预处理可显著抑制血清PNP活性和肝酶的升高。这些结果表明，LPS激活的Kupffer细胞损伤了肝窦内皮细胞，肝细胞损伤进展。地尔硫卓通过抑制细胞质和线粒体中钙浓度的升高来保护实验性内毒素血症中的肝细胞。然而，地尔硫卓似乎没有保护内皮细胞。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