The Protective Effects Of Ischemic Preconditioning And Postconditioning On Liver Ischemia/Reperfusion Injury In A Rat Model Of CO₂ Pneumoperitoneum

Objective : To investigate the protective effects of ischemic preconditioning and postconditioning on liver ischemia/reperfusion injury in a rat model of CO2 pneumoperitoneum(P).Method : 24 male SD rats were randomly divided into 4 groups, pneumoperitoneum (P group), ischemic preconditioning (IP group), ischemic postconditioning (IPo group) and control (C group). C group was subjected to sham operation. Other groups were subjected to the CO2 pneumoperitoneum, 15mmHg intra-abdominal pressure (IAP). P group was subjected to 60 min of P, followed by 30 min of deflation(D). IP group was subjected to preconditioning prior to P/D, which consisted of 10 min of P, followed by 10 min of D. IPo group was subjected to 60 min of P, followed by three cycles of 1 min of D and 1 min of P and 30 min of D. Plasma alanine aminotransferase(ALT) and aspartate aminotransferase(AST),as well as homogenized tissue malondialdehyde(MDA) and nitric oxide(NO) levels, glutathione(GSH) and superoxide dismutase(SOD) activities were measured respectively. The hepatic pathological changes were also observed by light microscopy. The expression of inducible nitric oxidesynthetase(iNOS) in liver tissue were examined by immunohistochemical technique in each group.Results: Plasma ALT and AST as well as liver MDA levels were significantly increased, whereas liver SOD values were decreased in groups P,IP and IPo, as compared to group C(P <0. 05). Plasma ALT,AST as well as liver MDA and NO levels were significantly decreased, whereas liver SOD and GSH values were increased in groups IP and IPo, as compared to group P(P <0. 05). The biochemical markers except GSH were no significant difference between group IP and IPo. The iNOS concentration markedly decreased in group IP and IPo in comparison with group P.CONCLUSIONS: ischemic preconditioning and ischemic postconditioning both can increase SOD and GSH levels and inhibit the expression of iNOS that can induce the production of NO, which may decrease hepatic I/R injury induced by CO2 pneumoperitoneum. Compared with IP, IPo increased GSH more prominently. It is suggested that IPo may play a greater role as protective effect on oxidative stress.