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A STUDY ON LIVER INJURY CAUSED BY LIVER ISCHEMIA AND SEPTICEMIA

肝缺血和败血症引起的肝损伤的研究

基本信息

批准号：
05671098
负责人：
ISOZAKI Hiroshi
金额：
$ 1.34万
依托单位：
OSAKA MEDICAL COLLEGE
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1995
项目状态：
已结题

项目摘要

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

间断或连续阻断肝血管行肝部分切除术后肝损伤的实验研究：正常和缺血肝，大鼠，总阻断时间为60 min，比较3种缺血方式后的肝损伤：15 min间歇夹闭组（I组）、30 min间歇夹闭组（II组）和60 min连续夹闭组（III组）。正常肝I、II组及肝硬化I组线粒体ATP、能荷恢复及磷酸化效率维持较好。因此，在进行肝硬化切除术时，应采用15分钟的间歇夹闭。钙拮抗剂维拉帕米对实验性内毒素血症大鼠肝细胞损伤有保护作用，钙拮抗剂维拉帕米对缺血性肝损伤有保护作用。 ...更多信息离子拮抗剂：用脂多糖（LPS）诱导大鼠实验性肝损伤（L-组），并同时注射地尔硫（LD-组）。在用氯化钆（GdC 13）预处理的大鼠中评估枯否细胞在LPS诱导的肝损伤中的参与。L-组线粒体内钙离子浓度升高，胞浆内钙离子浓度升高。LD组细胞浆和线粒体钙离子浓度明显降低。LD组血清肝酶升高和线粒体功能下降明显受到抑制。L组和LD组之间血清嘌呤核苷磷酸化酶（PNP）活性无差异。另一方面，GdC 13预处理显著抑制血清PNP活性和肝酶的升高。结果提示，LPS激活的枯否细胞损伤肝窦内皮细胞，肝细胞损伤进一步发展。地尔硫卓通过抑制细胞质和线粒体钙浓度升高来保护实验性内毒素血症期间的肝细胞。然而，地尔硫卓似乎没有保护内皮细胞。少