Effect Of Postconditioning With Propofol And Ischemia On The Hepatic Ischemia-reperfusion Injury In Rats

Objective To investigate the effect of postconditioning with propofol and ischemia on the hepatic ischemia-reperfusion injury at lipid peroxidation and apoptosis in rats. To investigate whether the protection of postconditioning with propofol and ischemia is better than single postcondtioning ways.Methods Thirty male SD rats weighing 200-250 g were randomly divided into 5 groups of 6 animals each: group I sham operation (S); group II I/R; group III ischemic postconditioning (IPC); groupⅣpropofol postconditioning (PPC) and group V IPC+PPC. All of these rats anesthetized by intraperitoneal injection 3% sodium pentobarbital (40 mg/kg). Hepatoduodenal ligament was separated after entry into the belly, the first porta hepatis was exposed and a rat local hepatic IRI model was established with reference to the previous method. Blood flow of median and left lobe of the liver was blocked with non-trauma mini artery clamp, causing 70% liver ischemia. However, the blood flow of right lobe was not blocked to prevent blood clot in portal vein and gastrointestinal tract. When the color of liver surface turn gray and the texture turn soft, the model of liver ischemic prepare to succeed. In groupⅡ-V the hepatic arteries and veins of middle and left lobes were occluded for 1 h followed by 4 h reperfusion. Ischemia of the liver was confirmed by the color of the liver turning from red to gray. In group III and V the livers were subjected to six episodes of 10 second ischemia at 10 second intervals at the end of 1 h ischemia before 4 h reperfusion. In groupⅣand V 0.5% propofol 10 mg/kg was given iv at the end of ischemia followed by propofol infusion at 40 mg·kg-1·h-1. Blood samples were taken at the end of 4 h reperfusion for determination of serum ALT activity. Mean-while liver specimens were taken for electron microscopic examination and determination of MDA content and SOD activity.Results I/R significantly increased serum ALT activity and MDA content in the liver and decreased liver SOD activity in group II. The I/R-induced changes were significantly attenuated by propofol and/or ischemic postconditioning in group III,ⅣandⅤ(P<0.05或P<0.01). I/R significantly increased Bcl-2 and Bax protein expression in the liver cells. Propofol and/or ischemic postconditioning increased Bcl-2 protein expression further but decreased Bax protein expression in group III,Ⅳand V as compared with groupⅡ(P<0.05或P<0.01). Electron microscopic examination showed that the pathologic changes induced by I/R were less severe in group III,Ⅳand V than in group I/R.Conclusions All of three postconditioning ways can reduced the hepatic I/R injury and the mechanism may be related to inhibition of lipid peroxidation and apoptosis, but the efficacy of propofol postconditioning is better than ischemia postconditioning at lipid peroxidation; propofol with postconditioning does not enhance the anti-lipid peroxidation and expression of protein Bcl-2/Bax compare with singal propfol and postconditioning...