Zhang Shun-Cai, Wang Wei, Ren Wei-Ying, He Bo-Ming, Zhou Kang, Zhu Wu-Nan
Department of Gastroenterology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China. zhangsc.zshospital.@net
World J Gastroenterol. 2003 Mar;9(3):534-8. doi: 10.3748/wjg.v9.i3.534.
To investigate the effects of cisapride on intestinal bacterial overgrowth (IBO), bacterial and endotoxin translocation, intestinal transit and permeability in cirrhotic rats.
All animals were assessed with variables including bacterial and endotoxin translocation, intestinal bacterial overgrowth, intestinal transit and permeability. Bacterial translocation (BT) was assessed by bacterial culture of MLN, liver and spleen, IBO by a jejunal bacterial count of the specific organism, intestinal permeability by determination of the 24-hour urinary (99m)Tc-DTPA excretion and intestinal transit by measurement of the distribution of (51)Cr in the intestine.
Bacterial translocation (BT) and IBO was found in 48 % and 80 % cirrhotic rats respectively and none in control rats. Urinary excretion of (99m)Tc-DTPA in cirrhotic rats with BT (22.2+/-7.8) was greater than these without BT (10.5+/-2.9). Intestinal transit (geometric center ratio) was significantly delayed in cirrhotic rats (0.31+/-0.06) and further more delayed in cirrhotic rats with BT (0.24+/-0.06) than these without BT (0.38+/-0.11). Cirrhotic rats with IBO had significantly higher rates of intestinal bacterial and endotoxin translocation, slower intestinal transit time and higher intestinal permeability than those without IBO. It was also found that BT was closely associated with IBO and the injury of intestinal barrier. Compared with the placebo group, cisapride-treated rats had lower rates of bacterial/endotoxin translocation and IBO, which was closely associated with increased intestinal transit and improved intestinal permeability by cisapride.
These results indicate that endotoxin and bacterial translocation in cirrhotic rats may be attributed to IBO and increased intestinal permeability. Cisapride that accelerates intestinal transit and improve intestinal permeability might be helpful in preventing intestinal bacterial and endotoxin translocation.
探讨西沙必利对肝硬化大鼠肠道细菌过度生长(IBO)、细菌及内毒素移位、肠道转运及通透性的影响。
对所有动物进行包括细菌及内毒素移位、肠道细菌过度生长、肠道转运及通透性等变量的评估。通过肠系膜淋巴结、肝脏和脾脏的细菌培养评估细菌移位(BT),通过特定生物体的空肠细菌计数评估IBO,通过测定24小时尿中(99m)锝-二乙三胺五乙酸排泄评估肠道通透性,通过测量(51)铬在肠道中的分布评估肠道转运。
分别在48%的肝硬化大鼠和80%的肝硬化大鼠中发现细菌移位(BT)和IBO,对照组大鼠未发现。有BT的肝硬化大鼠尿中(99m)锝-二乙三胺五乙酸排泄量(22.2±7.8)高于无BT的大鼠(10.5±2.9)。肝硬化大鼠的肠道转运(几何中心比)明显延迟(0.31±0.06),有BT的肝硬化大鼠比无BT的大鼠延迟更明显(0.24±0.06),无BT的大鼠为(0.38±0.11)。有IBO的肝硬化大鼠肠道细菌及内毒素移位率明显高于无IBO的大鼠,肠道转运时间更慢,肠道通透性更高。还发现BT与IBO及肠道屏障损伤密切相关。与安慰剂组相比,西沙必利治疗的大鼠细菌/内毒素移位率和IBO较低,这与西沙必利增加肠道转运和改善肠道通透性密切相关。
这些结果表明,肝硬化大鼠的内毒素和细菌移位可能归因于IBO和肠道通透性增加。西沙必利可加速肠道转运并改善肠道通透性,可能有助于预防肠道细菌和内毒素移位。