| Liver transplantation (LTx) has become the most effective treatment for the end stage of liver diseases. The donor shortage restricts liver transplantation from developing. The NHBD Liver graft suffers not only the warm ischemic injury but also the cold preservation and reperfusion injury. In the pathophysiological process, a number of cyokines, such as TNF- a , et . are releases with the activation of Kupffer cells, and the obstruction of microcirculation. The injuty of liver cells and sinusoidal endothelial cells (SEC) , which become the major cause of primary non-function (PNF). At present, the role of nitric oxide (NO) in ischemia-reperfusion injury was studied very popular. The inner-source NO can adjust liver circulation and resist the gathering of blood plates and the releasing of ET.TNF- a . The administration of L-Arg could increase the production of NO. Objective:In this study, the effect of L-Arg on the liver graft ischemia-reperfusion injury at different time-point after non-heart-beating (NHB) is observed and its mechanism is disscussed. The aim of this study is to investigate theory and experimental basis for using the NHBD reasonably and effectively. Methods:One hundred and four Wistar rats were randomly divided into seven groups. There are eight rats in the normal control group (N). The rest rats are devided into donors and recipients for orthotopic liver transplantation. In other six groups (sixteen rats in each group), LTx were performed between donors and recipients. These groups are as follows: experoimental control group 1 (Q), experimental group 1 (Ej), experimental control group 2 (C2), experimental group 2 (E2), experimental control group 3 (C3), experimental group 3 (E3). For CK E, group, C2, E2 group, C3, E3 group, the warm ischemic time is 0, 30, 45minutes respectively. Liver grafts were flushed with and preserved in 4C Euro-collins solution containing 1 mmol/L L-Arg for Ih in each experimental groups. Recipients of each experimental groups were injected with L-Arg 10mg/kg body weight by tail vein road 10 minutes before portal vein reperfusion. Donors and recipients of each experimental control were treated with physiological sodium chloride correspondingly. Then transplantationwas performed. At Ih, 3h, 24h after portal vein reperfusion, blood samples were obtained to determine the level of ALT, AST, TNF- a , ET. Three hours after portal reperfusion, grafts samples were fixed by 2.5% glutaradehyde for electronscopy observation. During operation, warm ischemic time and cold ischemic time, non-hepatic time and surgical operation time of recipient were recorded. Liver transplantation was not performed in normal control group. The samples were obtained with same method as used in other groups. Results:1. Cold ischemic time, non-hepatic time, surgical operation time among 6 groups were less discriminating (P>0.05).2. At Ih after portal vein reperfusion, the levels of ALT in both experimental groups (Els E2, E3) and experimental control groups (Cl5 C2, C3) were significantly increased than in normal control group (PO.05); At Ih, 3h, 24h, the levels of ALT in experimental groups (E,, E2, E3) were significantly lower than in correspondingly experimental control groups (C,, C2, C3) (P<0.05). The levels of ALT in group C3 were significantly higher than in group C, and C2 (PO.05), and the levels of ALT in group C3 were significantly higher than in group C2 (P<0.05).3. At Ih after portal vein reperfusion, the levels of AST in both experimental groups (E,, E2, E3) and experimental control groups(C1, C2, C3) were significantly increased than in normal control group (P<0.05); At 1h, 3h,2 4h, the levels of AST in experimental groups (E1, E2, E3) were significantly lower than in correspondingly experimental control groups (C1, C2, C3) (PO.05). The levels of AST in group C3 were significantly higher than in group C, and C2 (P<0.05), and the levels of AST in group C3 were significantly higher than in group C2 (P<0.05).4. At Ih after portal v...
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