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In cirrhosis, delayed intestinal transit may be responsible for increased endoluminal bacterial overgrowth and increased bacterial translocation. Octreotide has been reported to reduce intestinal transit. Therefore, we evaluated whether octreotide administration influences bacterial translocation in a model of liver fibrosis secondary to dimethylnitrosamine (DMNA) administration. Twenty-nine conscious rats were randomly assigned to three groups (sham rats + placebo as controls, DMNA + placebo, DMNA + octreotide, 1.5 microg/kg thrice daily subcutaneously), and including portal pressure, intestinal transit (radioactive method), and bacterial translocation were measured. Three of four variables measuring intestinal transit suggested a significant delay in intestinal transit in DMNA rats compared to controls (eg, cumulated radioactivity 50%: controls: 5.3+/-1.5, DMNA + placebo: 3.2+/-1.2, DMNA + octreotide: 2.7+/-1.9, P < 0.01). This delay tended to be enhanced by octreotide but the effect was only significant with one of the intestinal transit variables. Bacterial translocation was significantly increased in DMNA rats compared to controls but octreotide did not increase translocation [eg, germ count (log) in lymph nodes: controls: 3.1+/-3.6, DMNA + placebo: 12.3+/-4.4, DMNA + octreotide: 10.6+/-6.0, P < 0.001]. There was no significant correlation of portal pressure, intestinal transit, and bacterial translocation in this study. In conclusion, our results show that, although octreotide worsens delayed intestinal transit, it has no influence on the level of bacterial translocation.