Acute liver injury and hepatic failure are serious Acute liver injury is associated with a high rate of infectious and septic complications. Most of these infec-clinical conditions that are sometimes observed in extions are produced by gram negative enteric bacteria. tensive hepatic surgery and in patients with multiple We evaluated bacterial translocation, intestinal perme-system organ failure. 1,2 Bacterial infection and sepsis ability, blood flow, portal pressure, and intestinal mi-are recognized as dangerous complications of this remcroflora after induction of liver injury and 70% liver re-edy with significant share in its morbidity and mortalsection in the rat. The rate of translocation to both portal ity. [3][4][5] Gram-negative enteric bacteria are frequent and arterial blood was 100% at 24 hours and 50% at 48 causative organisms in most of the published studies. 6-8 hours after liver resection compared with 83% to portal It has been shown that the gut, as a reservoir of enteric vein and 50% to aortic blood at both time points after bacteria in the body, plays an important role in many acute liver injury. Translocation to intraabdominal orcritical clinical situations, such as major burns, hemorgans (liver, spleen, and mesenteric lymph nodes) was rhagic shock, and so on. 9 Under normal conditions a 100% in both groups at both 24 and 48 hours. The rate series of protective measures, such as mucosal barrier of translocation increased after liver injury at 48 hours with progression of the liver injury but was decreased function, immunoglobulin secretion, and local and sysin the 70% liver resection group with improvement of temic macrophage system prevent translocation of liver function. ''Total aerobic'' and ''total anaerobic'' bac-these potential pathogens to the extraintestinal sites. 10 terial counts in small intestine and cecum were not af-Severe clinical disorders may disrupt these normal profected. Pulmonary, distal small intestine, and cecal tective mechanisms and make it possible for the intestiblood flow were decreased in both groups, whereas nal bacteria to translocate. Translocation of endotoxin blood flow in the proximal small intestine was unaf-and intestinal bacteria in acute liver injury may intenfected. Portal pressure and flow were increased after sify the extent of injury and may also be responsible 70% liver resection, but they were decreased in acute for the high rate of associated infection and sepsis obliver injury. After acute liver injury, permeability of both served in these patients. So far, little attention has MATERIALS AND METHODSgery, Lund University, 221 85 Lund, Sweden. Experimental Groups.One hundred eight Sprague-