大鼠肠道缺血再灌注损伤后肠源性细菌内毒素移位的初步研究

Preliminary study of enterogenous bacteria endotoxin translocation after intestinal ischemia reperfusion injury in rats

目的 观察肠道I R损伤对肠源性细菌 内毒素移位的影响。方法 采用夹闭肠系膜前动脉(时间 6 0min)技术复制肠道I R损伤大鼠模型 :①检测血浆内毒素水平 (鲎试剂定量试验法 )和肿瘤坏死因子(TNFα) ,②肠系膜淋巴结、肝、肺、肾组织匀浆进行细菌培养。结果 研究成功地复制了肠道I R损伤大鼠模型 ,并观察到大鼠肠道I R损伤可引起 :①门、腔静脉血中内毒素水平明显升高 (P均 <0 .0 1) ,门脉血浆内毒素显著高于腔静脉血 (P <0 .0 1) ;②血浆TNFα在再灌注后 3h达峰值 ,明显高于缺血前水平 (P 均 <0 .0 1) ;③肠系膜各组淋巴结及肺、肝、肾组织匀浆均培养出细菌 ,且各组织中的细菌与回、盲肠腔内的优势菌分布相一致。结论 肠道I R损伤可引起小肠、盲结肠的细菌

Objective To study the effects of intestinal ischemia reperfusion injury on enterogenous bacteria and entotoxin translocation in rats.Methods Rat model of intestinal ischemis reperfusion injury was estalished with the clamping of the superior mesenteric artery for 60 minutes and then the clamping was relieved. The plasma level of endotoxin and TNFα was determined with limulus amebocyte lysate test and redioimmunoassay respectively. Bacteria in the lumen of the ileum and cecum and in the mesenteric lymph nodes, lungs, liver and kidneys were cultured with different media.Results After ischemia reperfusion injury, the plasma endotoxin level was significantly elevated in the caval and portal veins (P<0.01) and it was higher in the portal vein than in the caval veins (P<0.01). The plasma TNFα level reached the peak 72 hours after reperfusion and was significantly higher than the preischemic level ( P <0.01). The culture of the homogenate of all the groups of mesenteric lymph nodes, the lungs, liver and kidneys was positive for bacteria which similar to the distribution of the dominant bacteria in the lumen of the ileum and cecum.Conclusion Intestinal ischemia reperfusion can induce bacteria endotoxin translocation from the ileum and cecum.