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甲泼尼龙对失血性休克后肠屏障功能的影响 被引量:1

Influence of methylprednisolone on intestinal barrier function of rabbits after hemorrhagic shock
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摘要 目的探讨应用甲泼尼龙对失血性休克后肠黏膜屏障功能的影响。方法新西兰大白兔30只,随机分为失血性休克组、甲泼尼龙组、对照组。失血性休克采用股动脉放血制做模型,休克持续2h后回输失血及等量林格氏液复苏;甲泼尼龙组在复苏时静注甲泼尼龙50mg/kg一次;对照组不行放血处理。复苏后2h,留取血浆检测D-乳酸水平;取小肠组织行常规病理学检查,并制备肠组织匀浆测定其肿瘤坏死因子α(tumornecrosisfactor-α,TNF-α)和丙二醛(malondialdehyde,MDA)水平。结果失血性休克组肠黏膜结构破坏,血浆D-乳酸显著升高,肠组织匀浆中TNF-α和MDA水平增加。甲泼尼龙组上述指标均低于失血性休克组,差异具有统计学意义(P〈0.05)。结论早期大剂量使用甲泼尼龙对失血性休克后的肠屏障功能有保护作用。 Objective To investigate the effects of methylprednisolone on intestinal barrier function of rabbits after hemorrhagic shock. Method Thirty rabbits were randomly divided into three groups: control groups, hemorrhagic shock group, methylpredisolone-treatment group. Hemorrhagic shock was induced by modified Wiggers method until mean arterial pressure (MAP) was stabilized within 35 to 40 mmHg. The hypoteneion was maintained for 2 hours until the lossed blood was replenished with equivalent amount of Ringer's solution. A dose of 50 mg/kg methylpredisolone was given when methylpredisolone-treatment group began to be resuscitated. At 60 minutes after volume replenishment, rabbits were sacrificed. The content of D-lactate in the plasma was determined and the pathological changes of intestine were observed. At the same time, the levels of TNF-α and MDA in intestine homogenates were determined. Results Compared with control group, D-lactate, TNF-α and MDA were significantly increased in hemorrhagic shock group. As compared to hemorrhagic shock group, these levels were lower in methylpredisolone treatment group. The histopathologic changes were consistent with the biochemical markers, Conclusions Methylpredisolone could inbibit the increase in the levels of TNF-α and MDA in intestinal tissue, and have potential pretective effects on the intestinal barrier funtion in hemorrhagic shock.
出处 《中华急诊医学杂志》 CAS CSCD 2007年第3期267-269,共3页 Chinese Journal of Emergency Medicine
关键词 甲泼尼龙 失血性休克 肠屏障功能 Methylpredisolone Hemorrhagic shock Intestinal barrier funtion
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参考文献10

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