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PubMedDate not supplied

Effect of enteral nutrition of monoacetoacetin on bacterial translocation in burned rats.

BACKGROUND: Bacterial translocation (BT) occurs under stress, and enteral nutrition is said to be effective in counteracting this effect. The usefulness of i.v. nutrition of monoacetoacetine (MA) under stress has been reported previously, and we studied the effect of enteral nutrition of MA as it is related to BT. METHODS: Rats were given 13.6% MA or 15% glucose (Glu) via gastrostomy, and after 4 days a 30% full-thickness burn was made. Before and after administration of the burn, we measured serum cytokines; amounts of bacteria in the mesenteric lymph node (MLN), liver, and spleen (estimation of BT); mucosal thickness of the terminal ileum; and body weight changes. To confirm the effectiveness of MA in the small intestine, we estimated succinyl-CoA:3-oxoacid CoA-transferase (SCOT) expression in the terminal ileum by immunohistochemical staining and Western blot analysis. RESULTS: At 6 hours after burn, all cytokines were lower, and BT in the MLN was inhibited significantly in the MA group. Ileal mucosal thickness was not significantly different, but mucosa was more edematous in the Glu group. At 3 days after burn injury, BT was significantly inhibited in the MLN and liver, and the ileal mucosa was significantly thicker in the MA group. Body weight loss after burn injury was significantly smaller in the MA group. SCOT expression was the strongest at 6 hours after burn injury by Western blot analysis but not by immunohistochemical staining. CONCLUSIONS: Enteral nutrition of MA may be useful for the inhibition of intestinal mucosal atrophy and the prevention of multiple organ dysfunction syndrome caused by the inhibition of BT and subsequent overproduction of cytokines.

Acetoacetates↗
PubMed1993

The effect of biliary decompression on bacterial translocation in jaundiced rats.

Patients with obstructive jaundice are prone to septic complications after biliary tract operations. Restoring bile flow to the intestine may help to decrease the complication rate. The present study is aimed at evaluating the effect of biliary decompression on bacterial translocation in jaundiced rats. Sixty-six male Sprague-Dawley rats were randomly allocated to six groups subjected to common bile duct ligation (CBDL) and transection (groups 2-6) or sham operation (group 1). In groups 1 and 2 the incidence of enteric bacterial translocation was determined 2 weeks after sham operation or CBDL. In groups 3-6, biliary decompression was achieved by performing a choledochoduodenostomy after 2 weeks of biliary decompression. Bacterial translocation was then studied 1, 2, 3 and 5 weeks following biliary decompression. The rate of bacterial translocation to mesenteric lymph nodes in obstructive jaundice was significantly higher as compared with controls and decreased with time to nil three weeks following biliary decompression. The incidence of bacterial translocation was closely correlated (r = 0.844; p = 0.034) with serum alkaline phosphatase activity and seemed to fit with the morphological changes noted in the small intestine. The decrease in bacterial translocation, however, lags behind the recovery of liver function as measured by routine liver function tests and antipyrine clearance. Obstructive jaundice thus promotes bacterial translocation in the rat. Biliary decompression gradually decreases the rate of bacterial translocation.

Animals↗
PubMedDate not supplied

Hyperbaric oxygen prevents bacterial translocation in thermally injured rats.

This study was designed to evaluate the effects of hyperbaric oxygen (HBO2) on intestinal microflora and bacterial translocation (BT) caused by experimentally induced thermal injury in rats. Rats were separated into four groups, namely, HBO2 group, thermal injury (TI) group, TI + HBO2 group, and control group. All groups were further separated into short-term (2 days) and long-term (7 days) treatment or injury groups. Control group was neither exposed to thermal injury nor was given any treatment. Thirty percent second-degree thermal burn was induced on the dorsal body part of the rats in TI groups. In the HBO2 groups, rats received HBO2 treatment either without TI or following TI induction, for 2 and 7 days, respectively. Sampling from tissues and portal vein was performed on day 3 in the short-term groups and on day 8 in the long-term groups. Samples were cultured for identification of bacteria and colony counts. HBO2 treatment significantly reduced the colony counts of endogenous microflora in distal ileum of healthy rats (p < .05), while TI significantly increased the colony counts of endogenous microflora in distal ileum in short and long-term TI groups (p < .05). Presence of bacterial translocation was proven by bacterial isolation in mesenteric lymph nodes, liver, spleen and blood. Both short- and long-term HBO2 treatment following TI significantly reduced the colony counts of intestinal microflora (p < .05) and prevented bacterial translocation almost completely. It is concluded that thermal injury causes both bacterial overgrowth within intestinal lumen and bacterial translocation across the intestinal wall. HBO2 administration prevents both bacterial overgrowth and translocation.

Animals↗
PubMed2006

Treatment with Met-RANTES decreases bacterial translocation in experimental colitis.

BACKGROUND: During colitis, epithelial function is impaired, leading to increased bacterial translocation. Recent studies have shown the important role of proinflammatory cytokines and chemokines, including RANTES (regulated on activation, normal T-cell expressed and secreted), in inflammatory bowel diseases (IBDs). In this study, we evaluated the role of Met-RANTES, an antagonist of the RANTES receptor, on the impairment of bacterial translocation in a rat model of colitis. METHODS: Rats were randomly assigned to 3 groups. Group 1 = control, group 2 = experimental colitis, and group 3 = colitis plus Met-RANTES treatment. On day 7 after colitis was induced, plasma tumor necrosis factor-alpha colon tissue myeloperoxidase and portal blood endotoxin levels were measured. Lymph node, liver, and spleen culture quantified bacterial translocation. RESULTS: Met-RANTES treatment resulted in significant decreases in colonic damage as well as bacterial translocation in experimental colitis. CONCLUSIONS: These results suggest that chemokine receptor antagonists may potentially be useful in the treatment of IBDs.

Animals↗
PubMed2002

Hyperbaric oxygen ameliorates bacterial translocation in rats with mechanical intestinal obstruction.

PURPOSE: The aim of this study was to demonstrate bacterial translocation after experimentally induced intestinal obstruction as well as investigate the preventive effects of hyperbaric oxygen on obstruction-induced bacterial translocation in rats. METHODS: Forty Wistar-albino male and female rats were used. Although no procedure was done in the control group (n = 8), hyperbaric oxygen treatment under 2.5 atm absolute for 90 minutes daily was applied for two days in the hyperbaric oxygen group (n = 8). In the sham group (n = 8), after laparotomy the small bowel was only handled gently, and tissue sampling was done 48 hours later. In the obstruction group (n = 8) the ileum was ligated by 5-0 polypropylene just 5 cm proximal to the ileocecal valve. In the obstruction and hyperbaric oxygen group (n = 8), after obstruction hyperbaric oxygen treatment was applied. Forty-eight hours after the procedures, tissue samples from small bowel, mesenteric lymph nodes, spleen, and liver were taken and 1 ml of blood from the portal vein was withdrawn. All samples were cultured for microbiologic examination. RESULTS: Hyperbaric oxygen treatment significantly reduced the endogenous bacterial overgrowth in the small intestine of normal rats. Endogenous bacteria in the small intestine were significantly increased in the obstruction group, and the presence of bacterial overgrowth was proven by bacterial presence on mesenteric lymph nodes, spleen, liver, and blood. Hyperbaric oxygen treatment significantly reduced the endogenous bacterial overgrowth in the small intestine and prevented the bacterial translocation almost completely in obstruction-induced rats. CONCLUSIONS: Intestinal obstruction causes bacterial overgrowth and translocation. Hyperbaric oxygen treatment prevents the bacterial translocation effectively.

Animals↗
PubMedDate not supplied

The Caco-2 cell monolayer system as an in vitro model for studying bacterial-enterocyte interactions and bacterial translocation.

Partly because of inherent limitations of in vivo models, the cellular mechanisms underlying the process of bacterial translocation across the intestinal epithelial barrier are incompletely understood. We therefore used the Caco-2 intestinal cell line as an in vitro model to examine the bacterial translocation process under controlled conditions. Caco-2 cells were grown on porous membranes in the upper compartment of a two-compartment system. Caco-2 cells were cultured for 7, 14, 21, or 28 days. Cellular confluence and tight junction integrity were verified by measurements of dextran permeability and transepithelial electrical resistance. Bacterial translocation was measured by culturing the bacteria (E. coli C25) that were able to cross the Caco-2 cell monolayer. The passage of E. coli C-25 and dextran across the Caco-2 monolayer was higher and the transepithelial electrical resistance lower after 7 days of culture than after 14 or 21 days of culture. The Caco-2 cells became impermeable to dextran blue after 14 days of culture with an average transepithelial electrical resistance of 173.1 +/- 9.24 ohms.cm2. When increasing doses of (10(2)-10(9) colony-forming units) of E. coli were tested in 14-day-old Caco-2 monolayers, bacterial translocation occurred in a time- and dose-dependent fashion. Once cellular confluence and tight junction integrity have been established, bacterial translocation across Caco-2 cells appears to be a time- and dose-dependent process.

Cell Movement↗
PubMedDate not supplied

Effect of portal hypertension on bacterial translocation induced by major liver resection in rats.

OBJECTIVE: To evaluate the influence of portal hypertension on bacterial translocation from the gut caused by major hepatic resection. DESIGN: Randomised study. SETTING: University of Lund, Sweden. MATERIAL: 228 adult male Sprague-Dawley rats. INTERVENTIONS: Laparotomy and separation of the liver from its attachments (sham operated group), 70% hepatic resection, 90% hepatic resection, or subtotal ligation of the portal vein. For assessment of the degree of bacterial translocation a further laparotomy was done, 0.2 ml of blood taken from the portal vein and the vena cava, and specimens taken of mesenteric lymph nodes, liver, spleen, lungs, proximal jejunum, distal ileum, and transverse colon. Microcirculation of the intestine was measured by laser Doppler flowmetry with the probe held gently against the bowel wall at six points randomly chosen from the distal small intestine and colon. MAIN OUTCOME MEASURES: Alterations in portal venous pressure, arterial pressure, and bacterial translocation to other organs, particularly mesenteric lymph nodes. RESULTS: Bacterial translocation increased significantly after 90% hepatectomy, and there was an increase in portal pressure together with a decrease in systemic arterial pressure after both 90% hepatectomy and subtotal ligation of the portal vein. Subserosal blood flow to the distal small intestine decreased after 70% resection, 90% resection, and subtotal ligation of the portal vein; subserosal blood flow to the colon decreased only after 90% hepatectomy. CONCLUSION: Increased portal venous pressure after major hepatic resection is not the sole cause of the increase in the incidence of bacterial translocation from the gut in rats.

Animals↗
PubMedDate not supplied

Effects of fluid resuscitation, burn eschar excision, and blockade of afferent pain responses on bacterial translocation and acid-base balance after murine burn injury.

We tested effects of fluid resuscitation, early burn excision/grafting, and blockade of afferent stimuli from the burn wound on bacterial translocation and acid-base balance after murine burn injury. Burn excisions were performed with patients either 15 minutes or 2 hours after burn injury under anesthesia, and excised wounds were immediately closed with murine allograft skin. Twenty-four hours after 25% total body surface area (TBSA) burn injury and 48 hours after 32% TBSA injury, mesenteric lymph nodes were cultured. Incidences of bacterial translocation in 25% and 32% TBSA burns were 31.6% and 68.4% of animals, respectively. Burned animals were in severe shock, and metabolic acidosis reached a nadir 12 hours after burn injury, with base deficit -27.8 +/- 0.6 mEq/L; 5% to 10% of animals died acutely after burn injury. After excision/grafting of burned mice at 2 hours after burn injury, the incidence of bacterial translocation was unchanged (35.7% with 25% TBSA burn, 73.3% with 32% TBSA burn), and mortality did not change. When 32% TBSA excisions were performed exactly 10 minutes after burn injury, four of the 13 mice died within several hours, and five (55.5%) of the nine survivors translocated. Rates of bacterial translocation in mice receiving anesthesia or excision/grafting without burn injury were 15.0% and 20%, respectively (p = NS compared with normal mice). Subcutaneous implantation of normal or burned skin into normal animals neither elicited shock nor increased the incidence of bacterial translocation. Increasing amounts of fluid resuscitation in the 25% TBSA burn model provided only delayed improvement of acid-base balance; increased amounts of fluid did not decrease bacterial translocation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1995

A dietary nucleoside-nucleotide mixture inhibits endotoxin-induced bacterial translocation in mice fed protein-free diet.

Nucleosides and nucleotides are important substrates utilized by the intestinal mucosa. To determine the relative effect of dietary nucleosides and nucleotides on the gut, we investigated the effects of these compounds on endotoxin-induced bacterial translocation, cecal bacterial populations and ileal histology in protein-malnourished mice. There was an inhibition of gram-negative enteric bacteria in the mesenteric lymph node and spleen of the surviving mice fed the protein-free diet supplemented with a nucleoside-nucleotide mixture compared with the nonsupplemented group. Histologically, the damage to the gut mucosal barrier was more pronounced in the nonsupplemented group than in the nucleoside-nucleotide supplemented group. However, the cecal bacterial populations in the groups were not different. The villous height, crypt depth and total wall thickness were more developed in the supplemented group compared with the nonsupplemented group, indicating that the nucleoside-nucleotide mixture blocked bacterial translocation by preventing endotoxin-induced mucosal or epithelial damage. These results suggest that the nucleoside-nucleotide mixture could be used to inhibit or reduce the incidence of bacterial translocation, decrease intestinal injury and improve survival in a lethal model of protein deficiency and endotoxemia.

Animals↗
PubMedDate not supplied

Effect of oral genistein and isoflavone-free diet on cecal flora and bacterial translocation in antibiotic-treated mice.

BACKGROUND: There are several reports indicating that the isoflavone genistein may augment the integrity of the intestinal epithelial barrier as well inhibit bacterial internalization by cultured enterocytes. We speculated that oral genistein might enhance the integrity of the intestinal epithelial barrier as monitored by the extraintestinal dissemination of intestinal bacteria. METHODS: Mice were treated with oral antibiotics to induce cecal bacterial overgrowth accompanied by bacterial translocation of antibiotic-resistant enterobacteria, especially Escherichia coli. These mice were divided into separate groups that included chow-fed mice orally inoculated either with saline, vehicle, or genistein, and mice fed isoflavone-free diet and orally inoculated with either saline, vehicle, or genistein. Intestinal bacterial overgrowth was monitored by quantitative culture of excised ceca and bacterial translocation was monitored by quantitative culture of draining mesenteric lymph nodes. RESULTS: Mice fed the isoflavone-free diet had decreased populations of cecal bacteria compared with chow-fed mice, and bacterial translocation was reduced in chow-fed mice compared with mice fed isoflavone-free diet. However, bacterial translocation was similar in mice given oral genistein compared with appropriate control mice. CONCLUSIONS: Oral genistein had no noticeable effect on bacterial translocation in this model. However, the isoflavone-free diet had an antibacterial effect on cecal flora, and the isoflavone-free diet was associated with decreased numbers of cecal bacteria and decreased incidence of bacterial translocation.

Administration, Oral↗
PubMed1998

Evidence that aminoguanidine inhibits endotoxin-induced bacterial translocation.

BACKGROUND: The role of inducible nitric oxide synthase (iNOS) in endotoxin-induced bacterial translocation was investigated by using its specific blocker aminoguanidine in 46 albino mice (25-35 g) allocated into four groups. METHODS: The first group received intraperitoneal saline (control; 0.9 per cent w v(-1) sodium chloride 1 ml kg(-1); n=6), the second group intraperitoneal endotoxin (Escherichia coli lipopolysaccharide 055:B5 20 mg kg(-1); n=19), the third group intraperitoneal aminoguanidine (20 mg kg(-1), 20 min before and 12 h after saline; n=6) and the fourth group both endotoxin and aminoguanidine intraperitoneally (n=15). Some 24 h later, the animals were anaesthetized with ether and blood samples were collected by cardiac puncture together with mesenteric lymph node (MLN), spleen and liver specimens under aseptic conditions. Specimens were then cultured to determine the presence of colony-forming units as an index of bacterial translocation. RESULTS: No bacterial growth was detected in samples from the first and third groups. Colony-forming bacteria were found in ten of 14 MLN samples, eight of 14 spleens, four of 14 livers and three of 14 peripheral blood samples in the second group, with E. coli being the predominant pathogen. In contrast, in the fourth group, colony-forming bacteria were found in only three of 14 MLN samples (P=0.02 versus the second group), three of 14 spleens and one of 14 liver specimens. None of the values in the fourth group was significantly different from those in the saline control group. CONCLUSION: The inhibition of iNOS during endotoxaemia by its specific blocker aminoguanidine attenuates the incidence of bacterial translocation in mice. These results may be exploited clinically for the prophylaxis and treatment of septic states.

Animals↗
PubMed1995

Elemental diet and IV-TPN-induced bacterial translocation is associated with loss of intestinal mucosal barrier function against bacteria.

OBJECTIVE: The goal of the current study was to directly assess the role of loss of mucosal barrier function in nutritionally induced bacterial translocation. BACKGROUND: Parenteral and certain elemental enteral diets have been shown to promote bacterial translocation. The mechanisms underlying this observation, especially the question of whether nutritionally induced bacterial translocation is primarily related to loss of intestinal barrier function, versus an impaired immune system, remain to be fully elucidated. METHODS: Bacterial translocation was measured in vivo, ileal mucosal membranes were harvested, and their electrophysiologic properties and barrier function were measured ex vivo in the Ussing chamber system 7 days after receiving total parenteral nutrition solution parenterally (IV-TPN) or enterally (elemental diet). Chow-fed rats served as control subjects. RESULTS: The incidence of bacterial translocation was significantly increased both to the mesenteric lymph nodes in vivo and across the in vitro Ussing chamber-mounted ileal mucosal membranes of the elemental diet-fed and IV-TPN-fed rats. The magnitude of Escherichia coli and phenol red transmucosal passage in the Ussing chamber was significantly higher in the IV-TPN-fed rats than in the elemental diet-fed or chow-fed animals. The potential differences across the ileal membrane were similar between the three groups at all time points. However, the specific resistances of the ileal membranes of the IV-TPN and elemental diet groups were significantly less than the chow-fed animals, indicating increased membrane permeability. CONCLUSIONS: Loss of intestinal barrier function plays a major role in nutritionally induced bacterial translocation, and the loss of mucosal barrier function to both E. coli and phenol red appeared greater in the IV-TPN than the elemental diet-fed rats.

Animals↗
PubMedDate not supplied

Comparison of bacterial translocation during traumatic shock and hemorrhagic shock in rats.

UNLABELLED: Traumatic shock has been classified as a kind of hypovolemic shock similar to hemorrhagic shock. Since bacterial translocation has been observed in shock, this study investigated the difference in bacterial translocation during traumatic shock and hemorrhagic shock, and considered this effect on lung injury during sepsis. METHODS: Forty-eight male or female Sprague-Dawley rats were divided into 2 groups, hemorrhagic shock and traumatic shock. Bacterial translocation, endotoxin, and blood gas were evaluated. Alterations of the lungs morphologically and functionally were observed. RESULTS: Traumatic shock induced more bacterial translocation and endotoxemia from the gut. Blood gas analysis shows a more severe disorder in traumatic shock than in hemorrhagic shock. Pathological morphologic changes of lungs were more severe in traumatic shock than in hemorrhagic shock. CONCLUSIONS: Traumatic shock cause more bacterial translocation and endotoxemia which subsequently caused serial pathological alterations in lung morphologically and functionally than pure hemorrhagic shock does. These results suggest that this trauma activates more severe mechanism to damage lungs.

Animals↗
PubMedDate not supplied

Effect of three liquid diets on cecal bacterial flora and bacterial translocation in mice.

Separate groups of mice were fed either standard rodent chow or one of three liquid diets (Impact, Isosource HN, Fibersource HN) for 14 days to determine the effects of these liquid diets on the cecal bacterial flora and on the incidence of bacterial translocation to the mesenteric lymph nodes. Liquid Isosource and liquid Fibersource had no noticeable effect on either the cecal bacterial flora or the incidence of bacterial translocation. Liquid Impact was associated with cecal bacterial overgrowth but had no effect on the incidence of bacterial translocation. Each of the liquid diets was then lyophilized and similarly fed to mice; none of the lyophilized diets had a noticeable effect on the cecal bacterial flora or the incidence of bacterial translocation. To test these liquid and lyophilized diets in stressed mice, separate groups of mice were again fed the various diets for 14 days but given parenteral Escherichia coli lipopolysaccharide (LPS) 24 h before being killed. None of the liquid or lyophilized diets had a noticeable effect on the cecal bacterial overgrowth noticed in LPS-treated chow-fed mice. Compared with chow-fed mice, the typically elevated LPS-induced bacterial translocation was even more elevated in mice fed liquid diet but was somewhat decreased in mice fed lyophilized diet. Thus, the modulatory effects of these liquid diets on the cecal flora and the incidence of bacterial translocation appeared to depend on the composition of the diet and on prior treatment with parenteral LPS.

Animals↗
PubMed2005

A free radical scavenger, edaravone (MCI-186), diminishes intestinal neutrophil lipid peroxidation and bacterial translocation in a rat hemorrhagic shock model.

OBJECTIVE: To investigate the effects of edaravone, a novel free radical scavenger, on bacterial translocation induced by hemorrhagic shock. DESIGN: Prospective, randomized, unblinded animal study. SETTING: Surgical research laboratories of Shiga University of Medical Science. SUBJECTS: Male specific-pathogen-free Sprague-Dawley rats. INTERVENTIONS: The rats were randomly divided into three groups: conventional saline treatment, edaravone treatment, and sham shock induction. The saline and edaravone groups were subjected to hemorrhagic shock (mean arterial pressure of 30 mm Hg, for 30 or 60 mins). Rats were killed 30 or 60 mins after shock induction. Mesenteric lymph nodes were cultured for determination of bacterial translocation. Systemic plasma silkworm larvae plasma test, which can detect peptidoglycan and beta-glucan, and endotoxin tests were performed. Immunohistochemistry for 4-hydroxy-2-nonenal (4-HNE) was used to assess lipid peroxidation after shock. MEASUREMENTS AND MAIN RESULTS: The incidence and magnitude of hemorrhagic-shock-induced bacterial translocation to mesenteric lymph nodes were reduced by edaravone. Hemorrhagic-shock-induced increase of plasma silkworm larvae plasma test was also reduced by edaravone. Immunohistochemistry for 4-HNE showed many 4-HNE-positive cells in the lamina propria of the ileum 60 mins after hemorrhagic shock. Double immunohistochemistry revealed that many of these 4-HNE-positive cells were also myeloperoxidase positive. Moreover, the percentage of double-labeled cells with 4-HNE and myeloperoxidase in myeloperoxidase-positive cells was significantly lower in the edaravone group than in the saline group. CONCLUSIONS: The present findings suggest that lipid peroxidation of intestinal neutrophils is involved in bacterial translocation during hemorrhagic shock and that edaravone is potentially useful in diminishing bacterial translocation after hemorrhagic shock.

Animals↗
PubMed1995

Hyperosmotic glucose infusion during hemorrhage does not reduce bacterial translocation in 24 hour-starved rats.

Food deprivation 24 h before stress increases bacterial translocation in hemorrhage. Presently it tested whether hyperosmolality, induced by exogenous glucose infusion to improve plasma refill, prevents or reduces bacterial translocation after experimental hemorrhage in 24 h food-deprived rats. Rats were given an i.v. infusion of either 2 mL of 30% glucose (G) or the same volume of .9% NaCl (C) while simultaneously being submitted to a standardized 60 min hemorrhage period, of moderate or more severe hemorrhage. Blood was not reinfused. Despite development of marked hyperglycemia (p < .001, G vs. C) resulting in significantly greater reductions in packed cell volume (p < .001, G vs. C), bacterial translocation was detected similarly in both groups regardless of whether moderate (10/12-G, 9/12-C) or severe (15/19-G, 15/18-C) hemorrhage was inflicted. It was concluded that hyperglycemic hyperosmolality did not prevent bacterial translocation in these models of hemorrhagic stress in 24 h-starved rats.

Animals↗
PubMed2003

Effects of lactulose on intestinal endotoxin and bacterial translocation in cirrhotic rats.

OBJECTIVE: To investigate the effects of lactulose on intestinal bacterial overgrowth (IBO), bacterial translocation (BT), intestinal transit and permeability in cirrhotic rats. METHODS: BT in all animals was assessed by bacterial culture of mesenteric lymph node (MLN), liver and spleen, and IBO was assessed by a jejunal bacterial count of the specific organism. Intestinal permeability was determined by the 24-hour urinary (99m)Tc-diethylenetriamine pentaacetatic acid ((99m)Tc-DTPA) excretion, and intestinal transit was determined by measuring the distribution of (51)Cr in the intestine. RESULTS: BT and IBO were found in 48% and 80% of the cirrhotic rats, respectively, while not in the control rats. Cirrhotic rats with IBO had significantly higher levels of intestinal endotoxin higher rates of bacterial translocation, shorter intestinal transit time and higher intestinal permeability than those without IBO. It was also found that BT were closely associated with IBO and injury of the intestinal barrier. Compared with the placebo group, lactulose-treated rats had lower rates of BT and IBO, which were closely associated with increased intestinal transit and improved intestinal permeability by lactulose. CONCLUSIONS: Our study indicate that endotoxin and bacterial translocation in cirrhotic rats may attribute to IBO and increased intestinal permeability. Lactulose that accelerates intestinal transit and improves intestinal permeability might be helpful in preventing intestinal bacterial and endotoxin translocation.

Animals↗
PubMed2006

Gut flora and bacterial translocation in chronic liver disease.

Increasing evidence suggests that derangement of gut flora is of substantial clinical relevance to patients with cirrhosis. Intestinal bacterial overgrowth and increased bacterial translocation of gut flora from the intestinal lumen, in particular, predispose to an increased potential for bacterial infection in this group. Recent studies suggest that, in addition to their role in the pathogenesis of overt infective episodes and the clinical consequences of sepsis, gut flora contributes to the pro-inflammatory state of cirrhosis even in the absence of overt infection. Furthermore, manipulation of gut flora to augment the intestinal content of lactic acid-type bacteria at the expense of other gut flora species with more pathogenic potential may favourably influence liver function in cirrhotic patients. Here we review current concepts of the various inter-relationships between gut flora, bacterial translocation, bacterial infection, pro-inflammatory cytokine production and liver function in this group.

Antibiotic Prophylaxis↗