肝衰竭所致肠道菌群上移及易位

Hepatic failure inducedbacterial overgrowth and translocation in the upper GI tract

用细菌培养和菌落计数的方法对大鼠肝衰竭模型的胃肠道、胆道及肠系膜淋巴结内的细菌进行了检测；另对４例肝衰患者胃液进行细菌培养。结果显示，实验组大鼠消化道内细菌大量上移，胃、空肠、回肠内细菌含量分别为４．７×１０４／ｍｌ、２．１×１０５／ｍｌ、５．５×１０６／ｍｌ；对照组分别为４．６×１０２／ｍｌ、６．１×１０１／ｍｌ、２．４×１０３／ｍｌ，差异有显著性意义。实验组大鼠胆道及肠系膜淋巴结内均可培养到细菌。患者胃液中亦有大量细菌存在。病理学观察发现，肝衰竭大鼠胃肠胀气明显，肠壁松弛，管腔扩张；局部粘膜糜烂、出血；近端小肠粘膜病变最为明显。结论：肝衰竭时可以出现肠道菌群上移，引起胃肠胀气、内毒素吸收增加、细菌易位、消化道出血、自发性腹膜炎等。这种肠道菌群引起的内源性感染是肝衰竭最终导致多器官功能衰竭的始动原因。

In this report, microflora in GI tract and bacteria within bile duct and mesenteric lymphonodus in rat hepatic failure model was in investigated with a quantitative bacteria culture method. The histology of gastrointestine was also studied. The result shows that flora in the upper GI was significantly overgrew in the experiment group. The number of bacteria colonies in the specimens of stomach, jejunum and ileum were 4.7×10 4/ml, 2.1×10 6/ml, 5.5×10 6/ml in experiment group and 4.6×10 2/ml, 6.1×10 1/ml, 2.4×10 3/ml in control group respectively (P<0.01). The number of bacteria in jejunum was most significantly increased. Pathological injury was found in gastrointestinal mucosa and was also most severe in proximal small intestine. The structure of intestinal villi was decreased or almost disappeared; epithelial cells were degenerated and some even falled off; inflammavtory cells (mainly lymphocytes) in mucosa were increased. Mucosa erosion and bleeding would appear in some parts of alimentary tract, especially in the stomash. This result indicates that flourish flora in upper part of gastrointestine would produce a lot of gas in the lumen and induce pathological damage in gastrointestinal mucosa, and mediate abdominal distension, toxic intestinal expansion, alimentary tract haemorrhage. The proximal small intestine might be the most important position in which endotoxin is absorbed and bacteria is tranalocated.