Format

Send to

Choose Destination
See comment in PubMed Commons below
Am J Surg. 1990 Jan;159(1):79-84.

Obstructive jaundice promotes bacterial translocation from the gut.

Author information

  • 1Department of Surgery, Louisiana State University Medical Center, Shreveport 71130-3932.

Abstract

Experiments were performed to determine if obstructive jaundice promotes the translocation of bacteria from the gastrointestinal tract to visceral organs. Three groups of mice were studied: control (n = 20), sham ligated (n = 28), and bile duct ligated (n = 33). The sham-ligated group underwent laparotomy and manipulation of the portal region, whereas the ligated group had their common bile ducts ligated. Seven days later, the mice were killed, their organs cultured, and the gastrointestinal tract examined histologically. The bilirubin levels of the ligated group (18.7 mg/dL) were elevated compared with the other groups (0.5 mg/dL) (p less than 0.05). The incidence of bacterial translocation was higher in the ligated (33%) than in the control (5%) or sham-ligated (7%) groups (p less than 0.05). Since bile is important in binding endotoxin and maintaining a normal intestinal microflora, cecal bacterial populations were quantitated. The cecal levels of gram-negative, enteric bacilli were 100-fold higher in the bile duct-ligated mice in which bacterial translocation occurred (p less than 0.05), indicating that intestinal bacterial overgrowth was a major factor responsible for bacterial translocation. The mucosal appearance of the intestines from the control and sham-ligated groups was normal. In contrast, subepithelial edema involving the ileal villi was present in the ligated group. In conclusion, the absence of bile within the gastrointestinal tract allows intestinal overgrowth with enteric bacilli and the combination of bacterial overgrowth and mucosal injury appears to promote bacterial translocation.

PMID:
2136788
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center