AIM To investigate the effects of cisapride on intestinalbacterial overgrowth(IBO),bacterial and endotoxintranslocation,intestinal transit and permeability in cirrhoticrats.METHODS:All animals were assessed with variablesincluding bacterial and endotoxin translocation,intestinalbacterial overgrowth,intestinal transit and permeability.Bacterial translocation(BT)was assessed by bacterial cultureof MLN,liver and spleen,IBO by a jejunal bacterial count ofthe specific organism,intestinal permeability bydetermination of the 24-hour urinary ~(99m)Tc-DTPA excretionand intestinal transit by measurement of the distribution of~(51)Cr in the intestine.RESULTS:Bacterial translocation(BT)and IBO was foundin 48 % and 80 % cirrhotic rats respectively and none incontrol rats.Urinary excretion of ~(99m)Tc-DTPA in drrhotic ratswith BT(22.2±7.8)was greater than these without BT(10.5±2.9).Intestinal transit(geometric center ratio)wassignificantly delayed in cirrhotic rats(0.32±0.06)and furthermore delayed in cirrhotic rats with BT(0.24±0.06)than thesewithout BT(0.38±0.11).Cirrhotic rats with IBO hadsignificantly higher rates of intestinal bacterial and endotoxintranslocation,slower intestinal transit time and higherintestinal permeability than those without IBO.It was alsofound that BT was closely associated with IBO and the injuryof intestinal barrier.Compared with the placebo group,cisapride-treated rats had lower rates of bacterial/endotoxintranslocation and IBO,which was closely associated withincreased intestinal transit and improved intestinalpermeability by cisapride.CONCLUSION:These results indicate that endotoxin andbacterial translocation in cirrhotic rats may be attributed toIBO and increased intestinal permeability.Cisapride thataccelerates intestinal transit and improve intestinalpermeability might be helpful in preventing intestinal bacterialand endotoxin translocation. AIM To investigate the effects of cisapride on intestinalbacterial overgrowth (IBO), bacterial and endotoxinranslocation, intestinal transit and permeability in cirrhotic cells. METHODS: All animals were assessed with variablesincluding bacterial and endotoxin translocation, intestinalbacterial 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 ~ ) Cr in the intestine. RESULTS: Bacterial translocation (BT) and IBO was found in 48% and 80% cirrhotic rats respectively and none in non-controlling rats. Urinary excretion of ~ (99m) Tc-DTPA in drrhotic rats with BT (22.2 ± 7.8) was greater than these without BT (10.5 ± 2.9) .Intestinal transit (geometric center ratio) wassignificantly delayed in cirrhotic rats (0.32 ± 0.06) and where delay ed in cirrhotic rats with BT (0.24 ± 0.06) than thesewithout BT (0.38 ± 0.11) .Cirrhotic rats with IBO hadsificificantly higher rates of intestinal bacterial and endotoxinranslocation, slower intestinal transit time and higherintestinal permeability than those without IBO. It was alsofound 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 / endotox inranslocation and IBO, which was closely associated withincreased intestinal transit and improved intestinal permeability by cisapride.CONCLUSION: These results indicate that endotoxin andbacterial translocation in cirrhotic rats may be attributed toIBO and increased intestinal permeability. Capacitive thataccelerates intestinal transit and improve intestinal permeability may be beaten in intestinal bacterialand endotoxin translocation.