急性坏死性胰腺炎时肠屏障损害及肠源性细菌和内毒素移位的实验研究

目的 观察急性坏死性胰腺炎（ANP）时肠粘膜屏障的改变和肠源性细菌和内毒素移位。方法 将Wistar大鼠随机分为正常对照组（n=6)、假手术组（n=30)和ANP组（n=39)。采用人工胆汁胰管逆行灌注法制作ANP模型。观察胰腺、小肠病理改变和小肠粘膜上皮细胞间紧密连接（冷冻蚀刻电镜）变化。动态测定血浆D-乳酸、内毒素水平，以及腹腔脏器细菌移位率。结果 ANP后小肠粘膜损伤，皮皮细胞间紧密连接破坏甚至消失，血浆D-乳酸水平上升，发病早期即出现内毒素血症；ANP发生后72h脏器细菌移位率达到59.5%。结论 ANP早期肠粘膜屏障功能受损。导致肠道细菌和内毒素移位，成为全身炎症反应和胰腺继发感染的根源。

Damag to gut mucosal barrier and intestinal bacteria-end otoxin translocation in acute necrotizing pancreatitis rats

Objective To observe the changes in gut mucosal barrier and gut-origin bacteria-endotoxin translocation in acute necrotizing pancreatitis (ANP) rats. Methods Wistar rats were divided randomly into normal group (n=6), sham operation group (n=30) and ANP group (n=39). ANP was introduced by infusion of artificial bile into biliopancreatic duct. Morphology of pancreas and intestine were observed and tight junction on ileum epithelia were assessed by cryofracture replicas electroscopy. Plasma levels of D-lactic acid and endotoxin were examined at various time points. The rates of bacterial translocation to abdominal organs were also calculated. Results Mucosal and tight junction damages of the gut were found during early stage of ANP. Simultaneously, plasma D-lactate levels increased and endotoxemia occurred. The rate of bacterial translocation to organs was 59.5% 72h after ANP occurred. Conclusions Gut barrier function can be injured in the early stage of ANP, and resulting in gut origin bacteria-endotoxin translocation, which may be the originator of systemic inflammatory reaction and secondary infection of the pancreas.