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作 者:陈瑞华[1] 赵自刚[1] 牛春雨[1] 张静[1] 樊贵[1]
机构地区:[1]河北北方学院病理生理学教研室,河北张家口075029
出 处:《中国微循环》2008年第2期81-84,共4页Journal of Chinese Microcirculation
基 金:国家自然科学基金资助项目(No30370561);河北省自然科学基金资助项目(NoC2004000649)
摘 要:目的观察休克淋巴液对大鼠肠系膜微淋巴管内皮细胞(MMLEC)培养上清液中自由基、NO、TNFα、IL-6的影响,探讨休克淋巴液损伤MMLEC的体液机制。方法正常大鼠MMLEC进行原代培养,应用第三代MMLEC进行本研究。无菌条件下复制大鼠重症失血性休克模型(血压40mm-Hg,维持90min),引流休克时肠系膜淋巴液及门静脉血。以4%终浓度的休克淋巴液直接作用于MMLEC6h,同时以休克血浆、正常淋巴液、正常血浆、胎牛血清(FBS)、DMEM培养液作为对照;检测上清液中MDA、NO、TNFα、IL-6的变化。结果4%终浓度的休克淋巴液作用6h后,培养上清液MDA、NO、TNFα及IL-6含量均显著高于正常淋巴液组、休克血浆组、正常血浆组、FBS组以及DMEM组;而休克血浆作用MMLEC6h后MDA、NO及IL-6含量显著高于正常淋巴液组、正常血浆组、FBS组和DMEM组;其它组间无统计学差异。结论休克淋巴液诱导大鼠MMLEC损伤的体液机制与休克淋巴液诱导MMLEC自由基损伤、促进炎症介质释放有关。Objective To investigate the effect of shock lymph on free radicle, NO, TNFα and IL--6 in cultural supematant fluid of mesentery micro-lymphatic endothelial cells (MMLEC) of rats and to explore the humoral mechanisms of shock lymph damaging MMLEC. Methods The primary MMLEC was isolated, cultured and used at passage 3. The model of severe hemorrhagic shock was established by maintaining the blood pressure of rats at 40 mmHg for 90 min in aseptic condition and mesentery lymph and portal vein blood were taken out. The MMLEC was treated by shock lymph with 4% final concentration for 6 h, at the same time, the shock plasma, normal lymph, normal plasma, FBS and DMEM culture liquid were used as control. The contents of MDA, NO, TNFα and IL-6 in cultural supematant fluid were determined. Results After the MMVLC was treated by shock lymph at 4% final concentration for 6h, the contents of MDA, NO, TNFα and IL-6 in cultural supematant fluid of shock lymph group were significantly increased than those of shock plasma group, normal lymph group, normal plasma group, FBS group and DMEM group. And the contents of MDA, NO and IL-6 of shock plasma group were significantly higher than those of normal lymph group, normal plasma group, FBS group and DMEM group. There was no statistic difference among the normal lymph group, normal plasma group, FBS group and DMEM group. Conclusion The results demonstrated that the humoral mechanism of shock lymph damaging MMLEC might be related to the shock lymph inducing the free radical injury and increasing inflammatory mediator releasing.
关 键 词:休克 淋巴液 肠系膜微淋巴管内皮细胞 自由基 炎症介质
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