大鼠急性坏死性胰腺炎肠黏膜屏障功能障碍的观察

目的: 观察急性坏死性胰腺炎(ANP)大鼠肠黏膜屏障功能的变化。方法: SD大鼠80只随机分为假手术组(n=40)和ANP组(n=40)。胆胰管内逆行注射5%牛磺胆酸钠溶液制作ANP模型。观察大鼠胰腺和回肠的病理变化,动态测定肠脂肪酸结合蛋白(IFABP)、内毒素水平及肠系膜淋巴结和门静脉血细菌移位率。结果: 模型制作后2h血清IFABP明显升高,6h达到峰值(P<0.01),24h后降低。早期内毒素水平有明显升高,48h达到峰值(P<0.01)。肠系膜淋巴结细菌移位在ANP24h后明显升高,48h达到6/8只(P=0.013),门静脉血细菌移位48h达到3/8只(P=0.216)。结论: ANP早期肠黏膜屏障功能受损,引发肠道细菌和内毒素移位,IFABP可能是ANP早期肠黏膜屏障功能受损的预警指标。

An experimental study on the gut mucosal barrier dysfunction in rats with acute necrotizing pancreatitis

Objective:To observe the changes in gut mucosal barrier in rats with acute necrotizing pancreatitis(ANP).Methods:SD rats were randomly divided into sham operation group(n=40) and ANP group(n=40).The rat models of ANP were set up by retrograde injection of 5% sodium taurocholate in the biliopancreatic duct.The morphological changes of pancreas and ileum were observed.Plasma levels of intestinal fatty acid binding protein(IFABP) and endotoxin were examined at various time points,the bacterial translocation rates of mesenteric lymph nodes and portal vein were also examined at various time points.Results:The plasma levels of IFABP were elevated obviously 2 hours after ANP induction and reached peak value at 6 hours(P<0.01)and decreased at 24 hours.Plasma endotoxin levels also increased significantly at the early stage of ANP and reached peak value at 48 hours (P<0.01).The rates of bacterial translocation to mesenteric lymph nodes increased sharply 24 hours after SAP induction and reached six-eighths at 48 hours(P=0.013).The bacterial translocation rates of portal vein reached three-eighths at 48 hours(P=0.216).Conclusions:Gut mucosal barrier function can be injured in the early stage of ANP,and result in gut origin bacteria-endotoxin translocation,which may be the originator of septic and secondary infection of the pancreas.IFABP may be a specific marker for identification of gut mucosal barrier dysfunction in the early stage of ANP.