摘要
目的探讨急性脑缺血模型大鼠肠黏膜屏障应激性损害发生的机制。方法 64只雄性W istar大鼠随机分为缺血模型组和假手术对照组,两组大鼠分别按术后6、12、24和48 h时相点分为4个亚组(每组8只)。测定门静脉血内毒素(ET)、肿瘤坏死因子α(TNF-α)以及肠黏膜组织一氧化氮(NO)水平,检测肠系膜淋巴结等多器官组织匀浆中标记大肠杆菌的移位率。结果各时相点门静脉血ET、TNF-α以及肠黏膜组织NO水平模型组较对照组升高,P均<0.05;多脏器荧光标记大肠杆菌检出率模型组高于对照组,P<0.05。结论急性脑缺血模型大鼠伤后早期即有肠道细菌移位,与炎症介质和细胞因子水平的升高密切相关,是肠黏膜屏障损害的重要因素。
Objective To investigate the effect of inflammatory mediators and cytokines on the intestinal bacterial translocation in acute cerebral ischemia rats.Methods A total of 64 healthy male Wistar rats were divided into model group（n=32） and control group（n=32） randomly.Rats in each group were divided into four subgroups according 6,12,24 and 48 hours after operation（n=8）.Endotoxin（ET） and necrosis factor α（TNF-α） levels in portal vein blood and the nitric oxide（NO） level in intestinal mucosa were detected.E.coli displacement rate in mesenteric lymph nodes,liver,spleen,pancreas,lung and kidney tissues were marked and counted.Results The ET,TNF-α,NO levels and the positive rate of bacterial translocation in model group were obviously higher than those in control group（P0.05）.Conclusion High levels of inflammatory mediators and cytokines may play important roles for the intestinal bacterial translocation in acute cerebral ischemia rats,which induce the stress-related bowel mucosa barrier damage.
出处
《山东医药》
CAS
北大核心
2011年第20期10-12,共3页
Shandong Medical Journal
基金
首都医学发展科研基金获准资助项目(2007-3098)
关键词
缺氧缺血
脑
细菌移位
细胞因子
肠黏膜屏障
hypoxia-ischemia
brain
bacterial translocation
cytokines
intestinal mucosa barrier
