吗啡后处理对大鼠肝脏缺血再灌注损伤的影响

目的探讨吗啡后处理对大鼠肝脏缺血再灌注损伤的影响。方法32只雄性SD大鼠随机分为4组,假手术组（S组）：进腹后仅分离肝十二指肠韧带,不阻断肝门血管；缺血再灌注组（I/R组）：进行30 min的缺血及60 min的再灌注；缺血后处理组（IPO组）：缺血30 min时,进行30 s再灌/30 s再闭的3次循环,再全面恢复血液灌注；吗啡处理组（MPC组）：肝脏缺血30 min时,鞘内注射吗啡10μg/kg,后松开动脉夹全面恢复血液灌注60 min。各组于再灌注60 min时检测大鼠血清肝病酶学、超氧化物歧化酶（SOD）与丙二醛（MDA）的含量。结果 IPO组和 MPC组大鼠谷丙转氨酶（ALT）与谷草转氨酶（AST）含量均明显低于 I/R 组,且差异有显著性（P ＜0.01）；IPO组和 MPC 组血清中 SOD 的活性明显高于 I/R 组（P ＜0.01）；MDA 的含量显著低于 I/R 组（P ＜0.01）。结论吗啡后处理具有类似缺血后处理的肝脏保护作用,其机制部分可能与通过减少氧自由基的生成,增强肝脏的抗氧化能力有关。

Effect of Morphine Post-conditioning Against Hepatic Ischemia Reperfusion Inj ury in Rat

Obj ective]To explore the effect of morphine post-conditioning against hepatic ischemia reperfusion inj ury in rat.Methods]A total of 32 healthy male SD rats were randomly divided into 4 groups.The sham operated group （group S）only underwent the disassociation of duodenohepatic ligation without obstructing portal vessels.Ischemia reper-fusion group（I/R）underwent 30min ischemia and 60min reperfusion.Ischemic post-conditioning group（IPO）underwent 30s reperfusion and 30s reclosure for 3 cycles at 30min of ischemia,and then complete recovery of blood perfusion.Mor-phine post-conditioning group（MPC）underwent intrathecal injection of morphine 10ug/kg at 30min of liver ischemia,and then opening of artery clamp to completely recover blood perfusion for 60min..The serum concentrations of liver en-zyme,superoxide dismutase（SOD）and malondialdehyde（MDA）in rats of each group at 60min of reperfusion were meas-ured.Results]The levels of ALT and AST in IPO group and MPC group were obviously lower than those in I/R group, and there were significant differences（P〈0.01）.The activity of SOD in IPO group and MPC group was obviously high-er than that in I/R group（P〈0.01）.The level of MDA in IPO group and MPC group was significantly lower than that in I/R group（P〈0.01）.Conclusion]Morphine post-conditioning can protect liver like ischemic post-conditioning.The mechanism may be partly associated with the decreasing of oxygen free radical production and the increasing of hepatic an-tioxidation capability.