Male Sprague-Dawley rats were randomly divided into five groups in which group 1 received a sham operation (controls), groups 2-5 underwent common bile duct ligation and transection 14 days before the experiments. Two days prior to the studies, animals in groups 1 and 2 received saline orally, while groups 3–5 received an oral administration of either cholic acid, deoxycholic acid or whole bile. Specimens were taken for bacterial culture, and blood was collected for endotoxin assay. The rate of positive bacterial cultures from mesenteric lymph nodes in jaundiced salinetreated animals was significantly higher (p < 0.05) as compared with both controls and the other jaundiced animals treated with either bile or bile acids. Assays were positive for endotoxin in the jaundiced salinetreated group, whereas they were negative in both controls and bile- or bile-acid-treated animals. We conclude that oral administration of cholic acid, deoxycholic acid or whole bile inhibited bacterial translocation and endotoxin absorption in obstructive jaundice in the rat.

No abstract

Bacterial infections are frequent complications after liver resection. Of 138 patients who underwent major hepatectomy, 11 patients (8%) developed intra-abdominal sepsis in the postoperative period. Seven bacterial strains of gut origin were isolated from the abdominal cavity. Eight patients had multiple bacteria cultured. In the experimental studies on rat models, positive mesenteric lymph node cultures were seen 2 hours after removal of 70% and 90% of the total weight of the rat liver, and 12 hours after 50% hepatectomy, persisting for 3 and 4 days after 50% and 70% hepatectomy, respectively. The incidences of bacteremia 2 and 4 hours after 90% hepatectomy were 80% and 100%, respectively; 6 hours after 70% liver resection, the incidence of bacteremia was 33%. Blood cultures were positive in only 6% of the rats following 50% hepatectomy, and in none of the controls. Thus, bacterial translocation occurs in the early course after hepatectomy, the incidence being proportional to the amount of liver tissue removed.

It has been suggested that the gut plays a role in the development of bacterial complications, which are important contributors to morbidity and mortality in patients with acute pancreatitis. The present study evaluated the enteric bacterial translocation, bacterial homeostasis, and reticuloendothelial system function in experimental acute pancreatitis induced by intraductal injection of 5% sodium taurodeoxycholate in the rat. The incidence of bacterial translocation from the gut to mesenteric lymph nodes (MLNs) and lungs significantly increased after 12 hours and to the systemic circulation, ascites, and pancreas at 24 hours. The number of anaerobic bacteria and lactobacilli decreased in the colon and distal ileum from 6 or 12 hours, whereas the number of Escherichia coli increased from 12 hours. The systemic uptake rate of radiolabeled bacteria decreased from 6 hours after induction of acute pancreatitis. The uptake of radiolabeled bacteria by Kupffer cells decreased from 6 hours, whereas the uptake by macrophages from blood, lungs, and the intestine increased. A decrease in macrophage killing capacity was noted, reflected by an increase in the number of cultured viable bacteria from isolated macrophages. The whole-body oxygen extraction rate increased 4 to 24 hours after induction of pancreatitis, whereas the gut oxygen extraction rate decreased at 2 and 4 hours, followed by an increase at 12 to 24 hours. These data show that translocation of enteric bacteria occurs during the early stage of acute pancreatitis and that the MLN-thoracic duct-circulation may be a major route of bacterial dissemination. Compromised gut oxygen metabolism, overexaggerated intestinal macrophages, and impaired host immune function may be involved in the development of infectious complications associated with acute pancreatitis.

The process and route of bacterial translocation from the gut after major liver resection remain unclear. In the present study enteric bacterial translocation, enterocyte ultrastructure in the ileum and colon, the process and route of bacterial invasion and the permeability of the cell membrane system and blood-tissue barrier were evaluated in rats receiving sham operation, and 70 or 90 per cent hepatectomy. The incidence of bacterial translocation to mesenteric lymph nodes was 80-100 per cent in rats 6 h after 70 per cent and 2-4 h after 90 per cent hepatectomy, and 80-100 per cent to the systemic circulation 2-4 h after 90 per cent hepatectomy but only 20 per cent to the portal vein. An increase in bacterial adherence to the intestinal surface, damage to the permeability of the cell membrane system and blood-tissue barrier, and pathological alterations in the ileum and colon developed, correlating with the extent of liver removed and the time that had passed after hepatectomy. Most translocating bacteria appeared in morphologically intact enterocytes with increased membrane permeability, in antigen-presenting cells and in submucosal lymphatics, but some bacteria were also seen within damaged enterocytes 4h after 90 per cent hepatectomy. These results indicate that altered permeability of the cell membrane system may be one of the earliest characteristics of challenged enterocytes, and that enteric bacteria translocate through both morphologically normal and abnormal enterocytes. Translocation occurred mainly into the lymphatics, bacteria either being 'carried' by antigen-presenting cells or entering by active invasion.