急性坏死型胰腺炎时肠道细菌微生态改变与胰腺感染的实验研究

Experimental study on changes in intestinal microflora and bacterial translocation in acute necrotizing pan creatitis

目的：探索肠道生物屏障改变在胰腺感染中的作用。方法：１５只杂种犬在定植耐氨苄青霉素大肠杆菌（携带质粒ＰＵＣ１８的ＪＭ１０９）后，随机分组。胰腺炎组（８只）胰管内注入５％牛磺胆酸钠和胰蛋白酶引发急性坏死型胰腺炎，对照组（７只）仅作单纯剖腹术，７天后活杀。定量分析肠道粘膜及内容物中的菌群数，且对血液和内脏进行细菌培养。结果：胰腺炎组肠粘膜及内容物中大肠杆菌计数均高于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而双歧杆菌及乳杆菌均明显减少（Ｐ均＜０．０１）；肠粘膜厌氧菌／需氧菌比值严重倒置（Ｐ＜０．０５）；脏器和血培养结果：胰腺炎组所有动物均出现了肠道细菌易位，以肠系膜淋巴结和胰腺易位率最高（８７．５％～１００．０％），且能找到术前人工定植于肠道的耐药质粒菌。胰腺炎后第１天和第２天血培养阳性率分别为７５．０％和６２．５％，而对照组全部阴性。结论：急性坏死型胰腺炎时肠道出现明显的细菌微生态失调，以过度生长的Ｇ－杆菌为主的肠道细菌易位到胰腺及其它脏器，成为胰腺及胰周感染的根源。

Objective:To investigate the potential role of intestinal microflora barrier in the pathogenesis of pancreatic infection.Methods:Fifteen dogs were colonized with a strain of E.coli JM109 bearing ampicillinresistance plasmid PUC 18.The dogs were divided into two groups.In experimental group (n=8),acute necrotizing pancreatitis(ANP) was induced by injection of 0 5 ml/kg of sodium taurocholate with 3 000 U/kg trypsin into the pancreatic duct.The control group (n=7) underwent laparotomy only.All animals were sacrificed 7 days later.Mucosal and luminal microflora of intestine were analyzed quantitatively,and various organs were harvested for culturing.Results:In the experimental group,population levels of E.coli in the intestine were much higher than those of the controls,while bifidobacterium and lactobacillus were decreased significantly (all P <0 01),resulting in reversal of bifidobacterium/E.coli ratio as compared with the control group ( P <0 05).In addition,intestinal bacteria was isolated from organs of all animals in the experimental group,and JM109 was also detected in most cases.Positive blood culture was 75 0% and 62 5% on day 1 and day 2 after induction of ANP respectively,but no bacteria was found in the controls.Conclusions:This study confirms that microecological disturbance can take place in ANP ,and overgrowth of intestinal gramnegative bacteria may lead to translocation to the pancreas and other organs,becoming the source of pancreatic and peripancreatic infection.