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作 者:沈岩[1,2] 郑树森[1,2] 顾克洲[1,2] 孙义国[1,2] 李正之[1,2]
机构地区:[1]浙江医科大学附属一院普外科 [2]浙江医科大学微生物教研室
出 处:《中国普外基础与临床杂志》1998年第1期9-11,共3页Chinese Journal of Bases and Clinics In General Surgery
摘 要:为探讨肠源性感染的发生机理,将60只SD大鼠随机均分成肠梗阻组、环磷酰胺+肠梗阻组、环磷酰胺组和假手术组4组。回肠机械性肠梗阻24小时后取各组鼠腹腔液、门静脉血、心脏血、肠系膜淋巴结(MLN)和回肠末段内容物作细菌定量分析,同时测定门静脉血内毒素含量。结果显示:肠梗阻24小时即导致门静脉内毒素血症,肠内G-杆菌大量繁殖,肠菌移位于MLN中。免疫抑制剂环磷酰胺不仅增加肠梗阻时肠菌移位的发生率(100%∶80%),且使更多的肠菌存活于MLN中并向体循环内播散。由此表明,在免疫抑制状态下肠菌经淋巴途径侵入肠外组织。In order to investigate the mechanism of enterogenous infection, sixty SD rats were randomly allocated into four groups∶ group of intestinal obstruction; group of cyclophosphamide+intestinal obstruction; group of cyclophosphamide and group of sham operation. Each group included 15 rats. Twenty four hours after obstruction of the terminal ileum, the bacteria in blood of portal vein, blood of heart, peritoneal fluid, mesenteric lymph node (MLN) and content of gut were determined quantitatively, the concentration of endotoxin in portal system were measured. The results showed that early (24 hours) intestinal obstruction led to endotoxemia in portal vein, overgrowth of enteric G -bacili and bacterial translocation into the MLN. The immunosuppressive agent cyclophosphamide not only increased the rate of bacterial translocation into MLN and the number of living bacteria in MLN, but also promoted bacteria to spread into the systemic circulation. The authors conclude that under immunosuppression the bacterial translocation from gut by way of lymphatic channel plays an important role in enterogenous infection.
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