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肠系膜淋巴管结扎对休克大鼠肾功能不全的干预机制
引用本文:赵自刚,牛春雨,张静,陈瑞华,刘艳凯,张玉平,姜华,李继承.肠系膜淋巴管结扎对休克大鼠肾功能不全的干预机制[J].中国病理生理杂志,2008,24(4):743-748.
作者姓名:赵自刚  牛春雨  张静  陈瑞华  刘艳凯  张玉平  姜华  李继承
作者单位:1河北北方学院病理生理学教研室,河北 张家口 075029;2浙江大学细胞生物学研究所,浙江 杭州 310003
基金项目:国家自然科学基金 , 河北省自然科学基金 , 河北省科技攻关项目
摘    要:目的: 观察结扎肠系膜淋巴管对不同时期重症失血性休克大鼠肾组织自由基、炎症介质的影响,探讨肠淋巴途径对休克大鼠肾功能不全的干预机制。方法: 雄性Wistar大鼠78只,分为假手术组、休克组、结扎组。休克组与结扎组复制重症失血性休克模型,结扎组于休克复苏后行肠系膜淋巴管结扎术。于休克后90 min、输液复苏后0 h、1 h、3 h、6 h、12 h、24 h等时点处死大鼠,制备肾组织匀浆,检测MDA、SOD、NO、NOS、TNF-α、IL-6以及MPO水平,RT-PCR法测定各组大鼠肾组织iNOS mRNA表达。结果: 休克组大鼠输液复苏后不同时点肾组织匀浆MDA、NO、NOS、TNF-α、IL-6水平和MPO活性以及iNOS mRNA表达均有不同程度的升高,6 h-12 h持续在较高水平,均显著高于假手术组,肾组织匀浆SOD活性显著低于假手术组(P<0.01,P<0.05);结扎组输液复苏后6 h、12 h、24 h肾组织匀浆MDA、NO、NOS、TNF-α、IL-6水平和MPO活性以及iNOS mRNA均显著低于休克组相应时点,SOD活性高于休克组相应时点(P<0.01,P<0.05)。结论: 肠系膜淋巴管结扎干预重症失血性休克大鼠肾功能不全的机制与减少肾PMN扣押、降低TNF-α、IL-6的释放、抑制NO生成及iNOS mRNA表达、减少自由基释放与SOD消耗等因素有关。

关 键 词:休克  出血性  肾功能衰竭  肠系膜淋巴管  结扎术  炎症介导素类  
文章编号:1000-4718(2008)04-0743-06
收稿时间:2006-10-8
修稿时间:2006年10月8日

Mechanism of mesenteric lymph duct ligation against the renal insufficiency in hemorrhagic shock rats
ZHAO Zi-gang,NIU Chun-yu,ZHANG Jing,CHEN Rui-hua,LIU Yan-kai,ZHANG Yu-ping,JIANG Hua,LI Ji-cheng.Mechanism of mesenteric lymph duct ligation against the renal insufficiency in hemorrhagic shock rats[J].Chinese Journal of Pathophysiology,2008,24(4):743-748.
Authors:ZHAO Zi-gang  NIU Chun-yu  ZHANG Jing  CHEN Rui-hua  LIU Yan-kai  ZHANG Yu-ping  JIANG Hua  LI Ji-cheng
Affiliation:1Department of Pathophysiololgy, Hebei North University, Zhangjiakou 075029, China; 2Institute of Cell Biology, Zhejiang University, Hangzhou 310003, China. E-mail:ncylxf@126.com
Abstract:AIM: To observe the effect of mesenteric lymph duct ligation on free radical and inflammatory mediator in serious hemorrhagic shock rats at different periods, and explore the mechanism of intestinal lymphatic pathway on renal insufficiency. METHODS: 78 male Wistar rats were divided into the sham group, shock group, and ligation group. The model of serious hemorrhagic shock was established in shock group, ligation group, and mesenteric lymph was blocked by ligating mesenteric lymph duct in ligation group after resuscitating. All rats were executed and kidneys were taken out for making homogenate of 10 percent to determine levels of MDA, SOD, NO, NOS, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and myeloperoxidase (MPO) at time points after shock 90 min, after transfusion and resuscitate 0 h, 1 h, 3 h, 6 h, 12 h and 24 h. The expression of inducible nitric oxide synthase (iNOS) mRNA in kindey was detected by RT-PCR. RESULTS: The contents of MDA, NO, NOS, TNF-α, IL-6, MPO and iNOS expressions in renal homogenate of shock group were increased after transfusion and resuscitation, and were higher at 6 h and 12 h, and was significantly higher than that in sham group. The acvitity of SOD was significantly lower than that in sham group (P<0.01, P<0.05). The contents of MDA, NO, NOS, TNF-α, IL-6, MPO and iNOS expression in renal homogenate of ligation group after transfusion and resuscitation 6 h, 12 h and 24 h were significantly lower than those in shock group at same points, and the SOD activity was higher (P<0.01, P<0.05). CONCLUSION: The results demonstrate that the ligation of mesenteric lymph duct can antagonise the development of renal failure in serious hemorrhagic shock rats, and its mechanism might relate to reduce the PMN sequestration, decrease the levels of TNF-α and IL-6, inhibit NO production and expression of iNOS mRNA, suppress the release of free radical and consumption of SOD.
Keywords:Shock  hemorrhagic  Kidney failure  Mesenteric lymph duct  Ligation  Inflammatory mediators  Peroxidase
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