Intestinal transit and bacterial translocation in obstructive pancreatitis

Pancreatic infection from gut-derived bacteria has emerged as the major cause of death in necrotizing pancreatitis. Bacterial overgrowth of indigenous enteric organisms as a consequence of guts stasis (ileus) represents a potential initial event in this process. The present study was designed to exa...

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Bibliographic Details
Published in:Digestive diseases and sciences 1995-08, Vol.40 (8), p.1798-1804
Main Authors: Moody, F G, Haley-Russell, D, Muncy, D M
Format: Article
Language:English
Subjects:
Animals
Bacteria - growth & development
Colony Count, Microbial
Gastrointestinal Transit
Intestines - microbiology
Lymph Nodes - microbiology
Male
Mesentery
Pancreatitis - etiology
Pancreatitis - microbiology
Pancreatitis - physiopathology
Rats
Rats, Sprague-Dawley
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Summary:Pancreatic infection from gut-derived bacteria has emerged as the major cause of death in necrotizing pancreatitis. Bacterial overgrowth of indigenous enteric organisms as a consequence of guts stasis (ileus) represents a potential initial event in this process. The present study was designed to examine the interrelationships between intestinal transit, enteric bacteriology, and the translocation of bacteria from the gut lumen to mesenteric lymph nodes and splanchnic viscera during experimentally induced acute pancreatitis. Male rats underwent pancreaticobiliary duct ligation (PBDL) or sham surgery and were sacrificed after 24, 48, or 96 hr. Severity of pancreatitis was assessed with histology, tissue water content, and amylase and lipase levels. Intestinal transit was measured with fluorescent tracers. Blood, mesenteric lymph nodes (MLNs), splanchnic organs, and gut luminal contents were subjected to bacteriologic analysis. PBDL was followed by biochemical and histologic evidence of progressive pancreatic injury at each time interval. Enteric bacteria within the gut and in adjacent MLNs increased as intestinal transit decreased after PBDL-induced pancreatic inflammation. Surprisingly, all parameters returned to control levels by 96 hr in spite of progression of pancreatic inflammation.
ISSN:0163-2116
1573-2568
DOI:10.1007/bf02212705