己酮可可碱对重度失血性休克大鼠肝脏缺血再灌注后氧自由基的影响  

Effect of pentoxifylline on oxygen free radicals in liver as a result of ischemia-reperfusion in rats with severe hemorrhagic shock

作　　者：耿智隆[1] 陆化梅[1] 曹虹[1] 牛黎利[2] 徐鹏[1] 杨木强[1] 赵峰[1] 刘东[1] 

机构地区：[1]兰州军区兰州总医院麻醉科,兰州730050 [2]河南省洛阳正骨医院,河南洛阳471000

出　　处：《解放军医学杂志》2011年第3期221-224,共4页Medical Journal of Chinese People's Liberation Army

基　　金：全军"十一五"面上基金(06MA083)

摘　　要：目的探讨已酮可可碱(PTX)对重度失血性休克大鼠肝脏缺血再灌注后氧自由基的影响。方法 48只SD大鼠随机分为4组(n=12):对照组(C组)、单纯休克组(NR组)、乳酸林格液复苏组(LR组)及乳酸林格液联合PTX(25mg/kg)复苏组(LRPTX组)。采用改良Wiggers法制备失血性休克动物模型,分别于休克前(Ts)、处死前(Td)取静脉血检测谷丙转氨酶(ALT)及谷草转氨酶(AST)含量。NR组在休克后即刻、其余组在复苏后4h处死大鼠取肝组织测定过氧化物歧化酶(SOD)活性,丙二醛(MDA)含量,诱导型一氧化氮合酶(iNOS)及NF-κB蛋白表达情况。电镜及光镜下观察各组大鼠肝组织病理变化。结果与C组比较,NR组、LR组和LRPTX组Td时间点静脉血中AST及ALT水平均明显升高(P<0.05);肝组织MDAi、NOS含量明显升高,NF-κB蛋白表达增加,SOD活性降低(P<0.05)。肝组织病理学损伤明显。与LR组比较,LRPTX组静脉血中AST、ALT、MDAi、NOS含量均明显下降,NF-κB蛋白表达减少,SOD活性升高(P<0.05),肝组织病理学损伤减轻。结论 PTX可减少肝脏iNOS生成,抑制NF-κB活化,减少肝脏氧自由基生成,提高SOD活性,降低肝缺血再灌注损伤。Objective To investigate the effects of pentoxifylline（PTX） on oxygen free radicals in liver as a result of ischemia-reperfusion in rats with severe hemorrhagic shock.Method Forty-eight SD rats were randomly divided into four groups（12 each）： control group（C）,no resuscitation group（NR）,Ringer lactate solution（LR）-treatment group（LR）,and LR combined PTX（25mg/kg） group（LRPTX）.The rat model of severe hemorrhagic shock was established according to Wiggers method.Blood samples were collected at Ts（before shock） and Td（before sacrifice） for determination of AST and ALT.The rats were sacrificed and the livers were obtained for the determination of the activity of SOD,the contents of MDA and iNOS,and the expression of NF-κB immediately after shock in NR group and 4 hours after resuscitation in C,LR and LRPTX group.The pathological changes in the livers were observed with light microscope and electron microscope.Results Compared with C group,the AST and ALT levels in venous blood,the contents of MDA and iNOS,and the expression of NF-κB in liver were all significantly increased in NR,LR and LRPTX groups at Td time point,while the activity of SOD significantly decreased（P〈0.05）.There also showed signs of severe injury to the liver.Compared with LR group,the AST and ALT levels in venous blood,the contents of MDA and iNOS,and the expression of NF-κB were significantly decreased in LRPTX group,while the activity of SOD significantly increased（P〈0.05）.Pathologic changes of injury to the liver were significantly milder.Conclusion PTX can protect liver against ischemia-reperfusion injury by decreasing iNOS production and NF-κB activation,inhibiting the generation of oxygen free radical and enhancing the activity of SOD.

关 键 词：休克 出血性 再灌注损伤 活性氧 

分 类 号：R541.64[医药卫生—心血管疾病]