七氟醚对兔肝脏缺血再灌注损伤的影响

目的:探讨七氟醚对兔肝脏缺血再灌注损伤的影响.方法:将21只新西兰大白兔随机分为假手术组(S组)、肝脏缺血再灌注组(IR组)和七氟醚缺血再灌注组(Sev-IR组).S组仅行肝脏游离不阻断肝血流;IR组在夹闭肝门血管缺血45 min后再灌注60 min;Sev-IR组在七氟醚麻醉后,夹闭肝门血管缺血45 min后再灌注60 min.分别检测3组兔肝组织中丙二醛(MDA)、黄嘌呤氧化酶(XOD)的含量;HE染色观察肝组织形态学改变;免疫组织化学染色检测c-fos蛋白的表达情况.结果:肝缺血再灌注后,MDA、XOD含量均显著升高;光镜下见肝窦明显扩张、淤血,肝细胞明显水肿变性和空泡状变性,并有点状坏死;c-fos蛋白大量阳性表达.与IR组比较,Sev-IR组MDA、XOD含量均下降,差异均有统计学意义(P<0.05);肝细胞变性、坏死及肝血窦淤血减轻;肝组织c-fos蛋白表达量明显下调(P<0.05).结论:肝缺血再灌注损伤可使大量氧自由基释放,c-fos蛋白表达增加,引起肝组织的损伤;七氟醚可减轻肝缺血再灌注后肝组织损伤程度,可能与抑制再灌注后的过度氧化反应和减少c-fos蛋白表达有关.

Protective effects of sevoflurane on liver ischemia reperfusion injury in rabbits

Objective:To investigate the effects of sevoflurane on liver ischemia reperfusion injury in rabbits.Methods:Twenty-0ne rabbits were randomly divided into sham operation group(S),ischemia reperfusion group(IR) and sevoflurane ischemia reperfusion group(Sev-IR).Rabbits in IR group and Sev-IR group suffered from ischemia for 45 minutes and were followed by reperfusion for 60 minutes.Sev-IR group was anesthetized with sevoflurane.The concentrations of MDA and XOD of liver tissue were determined.The histopathologic changes in the liver were also observed.The expressions of c-fos protein were observed through immunohistochemisty.Results:The concentrations of MDA and XOD increased significantly after liver ischemia-reperfusion.The sinusoid was expanded and congestion obviously.The hepatic cells were hydropic degeneration and vacuole degenerated.Some of them were spotty necrosis.The protein of c-fos was positive expression.When using sevoflurane,the concentrations of MDA and XOD were statistical significantly decreased compared with IR group(P<0.05).The hepatic histopathological changes were improved.The degree of degeneration and necrosis of hepatic cells and the congestion of hepatic sinusoid lessened.The expression of c-fos was down regulated significantly(P<0.05).Conclusions:The injury of liver ischemia reperfusion can release mass oxygen radicals and increase the expression of c-fos.This can induce hepatic tissue injury.Sevoflurane can protect liver from ischemia reperfusion injury.Its possible mechanisms are restraining excess oxidizing reaction and decreasing the expression of c-fos protein.