Bacterial translocation in acute and chronic portal hypertension

• Published in: Hepatology (Baltimore, Md.) Md.), 1993-06, Vol.17 (6), p.1081-1085
• Main Authors: Garcia‐Tsao, Guadalupe, Albillos, Agustin, Barden, G. E., West, A. Brian
• Format: Article
• Language: English
• Subjects: Animals; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Blood - microbiology; Enterobacteriaceae - isolation & purification; Enterobacteriaceae - physiology; Gram-Negative Bacteria - isolation & purification; Human bacterial diseases; Hypertension, Portal - microbiology; Infectious diseases; Liver - microbiology; Lymph Nodes - microbiology; Male; Medical sciences; Rats; Rats, Sprague-Dawley; Spleen - microbiology
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.1840170622

Patients with cirrhosis are predisposed to develop spontaneous bacteremias and peritonitis, mainly by enteric bacteria. Portal hypertension, by producing congestion and edema of the bowel wall, could increase the passage of bacteria from the intestinal lumen to regional lymph nodes to the systemic circulation or to both, a process termed bacterial translocation. The aim of this study was to investigate bacterial translocation at two stages of experimental portal hypertension: (a) acute (when shunting is minimal); and (b) chronic (when shunting is extensive and mimics the portal hypertension of cirrhosis). Rats were killed 2 days (acute) or 15 days (chronic) after partial portal vein ligation or control surgeries. Samples of mesenteric lymph nodes, blood, liver and spleen for standard bacteriological cultures and a fragment of ileum for histological examination were obtained. Two days after surgery, a significantly greater proportion of rats with acute portal hypertension (12 of 13 or 92%) had positive mesenteric lymph node cultures compared with both control groups: sham‐operated (4 of 13 or 31%) and inferior vena cava–ligated (3 of 10 or 33%) animals (p < 0.01). However, 15 days after surgery no differences in translocation to mesenteric lymph nodes were found between rats with chronic portal hypertension (3 of 15 or 20%) and sham‐operated controls (3 of 11 or 27%). In neither the acute nor the chronic rats were bacteria isolated from blood, spleen or liver. Rats with acute portal hypertension had significantly greater mesenteric inflammation than rats with chronic portal hypertension and control animals. Results suggest that portal hypertension alone may not be a major factor in the development of spontaneous infections in cirrhosis and that other mechanisms, such as a defective immune system, may be more important. (HEPATOLOGY 1993;17:1081–1085.)