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PubMed2000

Inducible nitric oxide synthase gene knockout mice have increased resistance to gut injury and bacterial translocation after an intestinal ischemia-reperfusion injury.

OBJECTIVE: Intestinal ischemia-reperfusion after severe shock states is often associated with bacterial translocation and intestinal barrier dysfunction. Our previous studies showed that inducible nitric oxide synthase (iNOS) gene knockout mice were resistant to endotoxin-induced bacterial translocation and ileal mucosal damage. The goal of this study was to test whether iNOS mediates bacterial translocation after intestinal ischemia-reperfusion, using iNOS knockout mice (iNOS-/-) and their wild-type littermates (iNOS+/+). DESIGN: Prospective animal study with concurrent controls. SETTING: Small animal laboratory. SUBJECTS: Thirty-eight iNOS knockout mice and 51 wild-type littermates. INTERVENTIONS: iNOS+/+ mice or iNOS-/- mice were subjected to a sham operation or 30 mins of superior mesenteric artery occlusion followed by reperfusion. Twenty-four hours after reperfusion, bacterial translocation to mesenteric lymph nodes, ileal villous damage, and cecal bacterial population were evaluated. MEASUREMENTS AND MAIN RESULTS: Sham operation did not induce bacterial translocation, change cecal bacterial population levels, or cause ileal villous damage. Intestinal ischemia-reperfusion caused bacterial translocation in 72% of the iNOS+/+ mice but only 28% of the iNOS-/- mice. Both iNOS+/+ and iNOS-/- mice subjected to superior mesenteric artery occlusion (SMAO) in which bacterial translocation occurred had cecal bacterial population levels that were three logs higher than mice subjected to sham SMAO or mice subjected to SMAO in which bacterial translocation did not occur. The magnitude of villous injury was less in the iNOS-/- mice than the iNOS+/+ mice after SMAO, although the incidence of ileal villous damage was significantly higher in both the iNOS+/+ and iNOS-/- mice in which bacterial translocation occurred after SMAO than in the mice in which bacterial translocation did not occur after SMAO. iNOS+/+ mice subjected to SMAO had increased plasma concentrations of nitrite (NO2-) and nitrate (NO3-), and the plasma concentrations of NO2- and NO3- were highest in the mice in which bacterial translocation had occurred. CONCLUSION: iNOS knockout mice were more resistant to intestinal ischemia-reperfusion-induced bacterial translocation and mucosal injury than wild-type mice, suggesting that iNOS might play a role in intestinal ischemia-reperfusion-induced loss of gut barrier function.

Animals↗
PubMed2001

OK-432 reduces mortality and bacterial translocation in irradiated and granulocyte-colony stimulating factor (G-CSF)-treated mice.

Bacterial translocation/Acute radiation syndrome/Endotoxin/G-CSF/OK-432 Acute radiation induces bacterial translocation from the gut, followed by systemic infection and sepsis. In order to reduce the mortality after acute whole body irradiation, it is essential to control bacterial translocation. In this study, we established a bacterial translocation assay as a sensitive method to detect minor mucosal injury by radiation. By utilizing this assay, we evaluated the adverse effects, if any, of hematopoietic reagents on the mucosal integrity in the respiratory and gastro-intestinal tracts. Bacterial translocation to the liver and spleen occurred after whole-body irradiation if the dose exceeded 6 Gy. The administration of G-CSF unexpectedly increased the bacterial translocation in 8 Gy-irradiated mice. The pharmaceutical preparation of low-virulent Streptococcus pyogenes, OK-432, significantly reduced the endotoxin levels in peripheral blood without any reduction of bacterial translocation. A combined treatment with G-CSF and OK-432 decreased bacterial translocation and prevented death. This result indicates that the early administration of G-CSF has an adverse effect on bacterial translocation, and that a combined treatment of G-CSF and OK-432 attenuates the adverse effect of G-CSF and improves the survival rate after acute irradiation.

Animals↗
PubMedDate not supplied

The modulatory role of gut hormones in elemental diet and intravenous total parenteral nutrition-induced bacterial translocation in rats.

We have previously shown that parenteral and certain elemental diets promote bacterial translocation and that this diet-induced bacterial translocation can be prevented by the provision of bulk-forming dietary fiber. The goal of the current study was to test the hypothesis that fiber's protective effect on diet-induced bacterial translocation was mediated by trophic gut hormones. This hypothesis was tested by using bombesin (which stimulates gut hormone release) or the somatostatin analog Sandostatin (which inhibits gut hormone release) to modulate gut hormone release in rats receiving rat food, intravenous total parenteral nutrition, or an elemental diet. Both bombesin and fiber were effective in preventing elemental diet-induced bacterial translocation, whereas octreotide acetate abrogated the protective effect of fiber. Bombesin was also effective in limiting bacterial translocation in parenterally fed rats. Although both enteral (elemental diet) and parenteral diet-induced bacterial translocation were associated with cecal bacterial overgrowth, loss of small-bowel weight, and loss of mucosal protein content, none of these factors seemed to be primarily responsible for bacterial translocation. Because bombesin decreased the incidence of villous injury in the elemental diet-fed rats and decreased the incidence of villous injury and prevented loss of intestinal barrier function to horseradish peroxidase in the parenterally fed rats, it is possible that bombesin exerted its protective effect by limiting mucosal injury and preserving barrier function.

Animals↗
PubMed1998

The effect of an H2-receptor antagonist on small-bowel colonization and bacterial translocation in newborn rats.

Bacterial translocation (BT) is defined as the passage of enteric bacteria from the gastrointestinal tract to extraintestinal tissues. Bacterial overgrowth is one of the main promoting factors of BT, which is thought to play an important role in the pathogenesis of sepsis and necrotizing enterocolitis. It is believed that small-bowel colonization is established by bacterial spread through the rectum. Gastric acid is also involved in this process. An experimental study was designed for investigating the effect of gastric acid inhibition with the use of an H2-receptor antagonist on intestinal colonization and BT in newborn rats. Animals were divided into two groups: the ranitidine group (n = 20) received ranitidine 10 mg/kg per day intramuscularly for 5 days; the control group (n = 30) received saline solution. Mesenteric lymph node, spleen, liver, stomach, small bowel/cecum, and large bowel specimens were obtained from each rat 5 days later and gram-negative and -positive aerobic bacteria identified by the use of chocolate and Endo agar. It is concluded that: (1) there was a strong correlation between gastric and small-bowel bacterial colonization in the ranitidine group; (2) no correlation between large-and small-bowel colonization could be demonstrated; and (3) BT occurred only in the ranitidine group.

Animals↗
PubMed2001

Tumour necrosis factor mediates bacterial translocation after haemorrhagic shock and endotoxaemia.

OBJECTIVE: To assess the extent of bacterial translocation after haemorrhagic shock and reperfusion, and the involvement of tumour necrosis factor (TNF) in its mediation. DESIGN: Controlled, randomised prospective experiment. SUBJECTS: 87 rats in 7 groups. INTERVENTIONS: Haemorrhagic shock was induced in rats for 1 hour. Endotoxaemia was induced in a second group by the injection of lipopolysaccharide. A third group was injected with exogenous TNF. Some of the animals were further treated with anti-TNF. MEASUREMENTS: After 24 hours, bacterial translocation in blood and in several remote organs, and serum TNF concentrations were measured. RESULTS: High bacterial counts were found in all remote organs of rats with haemorrhagic shock or endotoxaemia. Their serum TNF concentrations were significantly higher than in the corresponding sham-operated controls. Anti-TNF significantly reduced the extent of bacterial translocation. Rats, the only treatment of which was exogenous TNF, developed substantial bacterial translocation. CONCLUSION: Bacterial translocation is associated with increased serum TNF, and can be minimised by anti-TNF. This, and the triggering of translocation in unprovoked animals by TNF alone, suggest that TNF may be the stimulator, and not the consequence, of bacterial translocation.

Animals↗
PubMed2005

Green fluorescent protein labeling Escherichia coli TG1 confirms intestinal bacterial translocation in a rat model of chemotherapy.

It has been reported that treatment with methotrexate (MTX) induces intestinal bacterial translocation; however, the definitive evidence of intestinal bacterial translocation induced by MTX has been lacking. The aim of this study was to confirm the intestinal bacterial translocation caused by MTX and to evaluate the preventive effect of granulocyte colony-stimulating factor (G-CSF) on intestinal bacterial translocation caused by MTX. Sprague-Dawley rats were treated with MTX (3.5 mg/kg) for 3 days to induce intestinal bacterial translocation; with gavaged Escherichia coli TG1 labeled with green fluorescent protein (GFP) for 2 days to track intestinal bacterial translocation; and with G-CSF (10 mug/kg) for 4 days to prevent intestinal bacterial translocation. Representative tissue specimens from the mesenteric lymph nodes, spleen, liver, and kidney were aseptically harvested for bacteria culture in ampicillin-supplemented medium. The bacteria labeled with GFP were detected in tissue specimens harvested from the rats treated with MTX but not detected in the rats that were not treated with MTX. G-CSF significantly ameliorated the situation of intestinal bacterial translocation.

Animals↗
PubMedDate not supplied

Effect of plaunotol on bacterial translocation in the rat small intestine.

BACKGROUND AND AIMS: Bacterial translocation is precipitated by an increase in bacteria or endotoxin, depression of the membrane barrier, and an increase in mucosal permeability. Plaunotol is a mucosal protective agent, and observed to have a strong suppressive effect on superoxide production. In this study, the effect of plaunotol on bacterial translocation was examined using the model of ischemia and reperfusion. METHOD: Male Sprague Dawley rats were used to create the following model for evaluation of bacterial translocation: (i) the control group; (ii) the preventive dose group (plaunotol 30 mg/kg/day one week before surgery); (iii) the therapeutic dose group (plaunotol 30 mg/kg/day one week after surgery); and (iv) the full dose group (plaunotol 30 mg/kg/day one week before surgery and one week after surgery). Bacterial translocation was assessed as the blood concentration of the endotoxin. RESULTS: In the control group, the endotoxin increased significantly 3 days postsurgery (13.7+/-5.6 pg/ml) compared with before surgery (1.1+/-0.1 pg/ml). In the preventive and full-dose groups, the erndotoxin decreased significantly 3 days postsurgery (4.4+/-2.8 pg/ml, 5.7+/-2.7 pg/ml, respectively) compared with that of the control group. CONCLUSION: Plaunotol in the preventive and full-dose groups decreased the endotoxin. This suggests that plaunotol is one of the protectors for bacterial translocation.

Animals↗
PubMed1997

Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by D-galactosamine.

BACKGROUND/AIM: Bacterial infections and sepsis are frequent complications of acute liver injury, with a high share in the mortality and morbidity of this condition. Bacterial translocation from the gut may play an important role in the high rate of infections observed. In this experiment the effect of different oral supplementation on bacterial translocation was evaluated in acute liver injury induced by D-galactosamine in the rat. METHODS: Rats were given oral supplements of lactulose, neomycin, Lactobacillus reuteri R2LC, and Lactobacillus plantarum DSM 9843 for 1 week. Liver injury was induced by intraperitoneal administration of 1.1 g/kg D-galactosamine. Twenty-four hours later, rats were sacrificed and liver enzymes and histology, intestinal bacterial count and microflora, intestinal mucosal histology, DNA and RNA content, bacterial translocation to blood, mesenteric lymph nodes, and liver, and serum endotoxin were studied or measured. RESULTS: Lactulose was highly effective in prevention of liver injury and bacterial translocation. Neomycin and Lactobacillus plantarum DSM 9843 showed a moderate effect in prevention of liver injury and bacterial translocation. Intestinal bacterial count and microflora were affected by different treatment modalities. No endotoxin concentration was found in any of the experimental groups. Both lactobacilli could significantly improve the mucosal proliferative state. CONCLUSIONS: Oral supplementation of lactulose with anti-endotoxin effect could successfully prevent the liver injury and the subsequent bacterial translocation in acute liver injury induced by administration of D-galactosamine in the rat. This effect was irrespective of the intestinal bacterial alteration or mucosal proliferative state.

Acute Disease↗
PubMedDate not supplied

Effects of a water-soluble ethylhydroxyethyl cellulose on gut physiology, bacteriology, and bacterial translocation in acute liver failure.

Bacterial infection and bacteremia are common complications in patients with acute liver failure. Bacterial translocation from the gut has been suggested to be a major cause of bacterial infections in experimental acute liver failure. In the present study, a water-soluble ethylhydroxyethyl cellulose (EHEC) was administered orally 1 and 24 hours prior to 90% hepatectomy in the rat in order to prevent bacterial translocation in experimental acute liver failure induced by subtotal liver resection in the rat. Ninety percent hepatectomy alone resulted in 80 to 100% translocation to mesenteric lymph nodes or blood 2 and 4 hours after operation. There was no translocation in rats undergoing sham operation or 90% hepatectomy with EHEC administration prior to operation (p < .01). Bacterial overgrowth, increased bacterial adherence onto the intestinal surface, and diminished intestinal and mucosal mass were also observed in animals with subtotal liver resection, but not in those administered EHEC. A delayed 2-hour intestinal transit time occurred in both groups receiving subtotal liver resection, with or without oral EHEC. EHEC inhibited bacterial growth and DNA synthesis and altered bacterial surface properties after 1-hour incubation with bacteria in vitro, an interaction that was not further influenced by time. These results imply that EHEC may alter enterobacterial capacities of metabolism, proliferation, and invasion by effects on the bacterial surface. Furthermore, EHEC seems to possess a trophic action on the intestine, though without enhancing the intestinal motility.

Acute Disease↗
PubMed2002

Bacterial translocation following intrabdominal surgery. Any influence of antimicrobial prophylaxis?

Bacterial translocation may accompany various intra-abdominal operations. In order to define its incidence and the effect of preoperative antimicrobial prophylaxis and the duration of hospitalization before elective surgery, mesenteric lymph nodes were excised from 43 patients undergoing various programmed intra-abdominal operations without any evidence of intra-abdominal septic focus. Nodes were cultured and examined for histopathological findings of reactive lymphadenitis. The incidence of bacterial translocation was 5.9% accompanying graft replacement post aortic aneurysm, 44.4% accompanying colectomy, 50% accompanying gastrectomy and 33.3% accompanying splenectomy but it did not occur with other types of laparotomy. Bacterial isolates from the mesenteric lymph nodes were mainly species of enterobacteriaceae. Bacterial translocation was found in 17.6% of patients receiving antimicrobial prophylaxis prior to dissection of the lymph nodes compared with 26.8% of those administered prophylaxis after lymph node removal (PNS). Reactive lymphadenitis was documented in 70.6% of patients undergoing aortic aneurysm graft replacement, in 33.3% undergoing colectomy, in 50% undergoing gastrectomy, in 33.3% undergoing cholocystectomy (33.3%) whereas it was not found in any patient undergoing splenectomy or other type of laparotomy. It is concluded that colectomy and gastrectomy are accompanied by the greatest risk for bacterial translocation among a great variety of intra-abdominal operations. The administration of preoperative antimicrobial prophylaxis and the duration of hospitalization before operation did not seem to have any effect on the process of bacterial translocation.

Abdomen↗
PubMed1996

The microenvironment influences the pattern of bacterial translocation in formula-fed neonates.

The authors previously demonstrated that neonatal rabbits fed conventional formula have a significantly greater incident of bacterial translocation than do neonatal rabbits fed breast milk. They hypothesized that exogenous bacteria in the formula and/or the microenvironment of the neonatal rabbit may contribute to the higher incidence of bacterial translocation. In the present study, the authors examined the incidence of bacterial translocation in neonatal rabbits fed pasteurized formula, unsterile formula, or breast milk while being housed in a clean or unsterile environment. The rabbits were divided into five groups. Groups I and II were fed pasteurized formula; groups III and IV were fed unsterile formula. In addition, groups I and III were housed in a clean environment, and groups II and IV were kept in an unsterile environment. The neonates in group V were fed breast milk and were kept in an unsterile environment. On the seventh day, the animals were killed, and the mesenteric lymph nodes, liver, and spleen were cultured for the presence of bacteria. Bacterial translocation occurred in 100% of group IV neonates. A clean environment (groups I and III) eliminated gram-negative bacterial translocation. A reduction (50%) in the overall incidence of bacterial translocation was obtained by pasteurizing the formula (group I v group III). Group II had significantly less gram-negative bacterial translocation than did group IV. None of the neonates in group V had translocation. The data show that a clean environment abrogates gram-negative bacterial translocation. Pasteurizing the formula significantly reduces the incidence of gram-negative bacterial translocation, and further reduces overall bacterial translocation in a clean environment. The authors hypothesize that control of the microenvironment can significantly influence the pattern of bacterial translocation in formula-fed neonates, and thus potentially reduce the incidence of gut-origin sepsis. Factors present in breast milk inhibit bacterial translocation, regardless of the microenvironment.

Animals↗
PubMed2003

HPA axis activation and neurochemical responses to bacterial translocation from the gastrointestinal tract.

Stress can cause migration of indigenous bacterial flora from the gut to the peritoneum, a phenomenon known as bacterial translocation. Destruction of the cell walls of gram-negative bacteria can result in the production of endotoxin (lipopolysaccharide, LPS), which is the likely cause of sepsis. Exogenously administered LPS can activate the hypothalamo-pituitary-adrenal (HPA) axis as well as brain noradrenergic and indoleaminergic systems. Thus, it is possible that activations of these systems associated with laboratory stressors in rats and mice could be attributed to bacterial translocation and LPS production. To test this hypothesis we conducted experiments on the time course of bacterial translocation in response to restraint in mice, while measuring HPA and neurochemical responses. These experiments failed to show good correlations between the occurrence of bacterial translocation and HPA and neurochemical activations, suggesting that the later responses were not linked to bacterial translocation. This conclusion was supported by the observation of normal neurochemical responses to restraint in germ-free mice. In further experiments, translocation of Salmonella typhimurium, a bacterium that readily translocates in unstressed animals, was associated with HPA activation and noradrenergic and indoleaminergic responses, indicating that bacterial translocation can indeed activate the HPA axis and brain amines. However, the above experiments suggest that this is not the mechanism by which restraint activates these systems.

Animals↗
PubMed2005

Variability of bacterial translocation in the absence of intestinal mucosal damage following injury and the influence of interleukin-6.

Bacterial translocation and intestinal mucosal damage have been reported as potentially clinically important sequelae of injury. Evidence that endogenous interleukin-6 (IL-6) is able to protect against infection, and that orally administered IL-6 could prevent bacterial translocation and mucosal damage following haemorrhage, led us to evaluate the impact of injury on the intestinal mucosa and the role of endogenous IL-6. Normal and IL-6-deficient (IL-6-/-) mice were subjected to haemorrhage of increasing severity, hind limb ischaemia, or both. Mucosal integrity and bacterial translocation to the liver, spleen and mesenteric lymph nodes (MLN) were examined after 16 h. Bacterial translocation to each of these tissues was observed in unoperated animals. The more severe haemorrhage procedures, and hind limb ischaemia, increased bacterial translocation to the liver significantly in most experiments with normal mice. The IL-6-/- mice survived the most severe haemorrhage procedure less well (p = 0.0015), although increased bacterial translocation was not seen. There was no clear evidence of mucosal damage, or bacterial translocation to spleen and mesenteric lymph nodes, in either normal or IL-6-/- mice. Intestinal IgA concentrations were the same in IL-6-/- mice and controls. These data demonstrate that increased bacterial translocation can be observed following severe injury, but that neither bacterial translocation nor severe injury are inevitably associated with morphological damage to the intestinal mucosa, and endogenous IL-6 is more likely to promote bacterial translocation than protect the gut.

Journal Article↗
PubMed2002

The effects of pentoxifylline on bacterial translocation after intestinal obstruction.

Bacterial translocation (BT) occurs mainly in preseptic conditions such as intestinal obstruction, trauma, and burn, and the underlying mechanisms are still unclear. Pentoxifylline (PTX) is a derivative of methyl xanthine and has several beneficial effects in sepsis. We investigated the effects of PTX on a rat BT model. Simple intestinal obstruction (IO) was choosen to create high BT rates. Rats were divided in to five groups of 10 rats. Either 50 mg/kg PTX or placebo (3 mg/100 g saline) was administered subcutaneously following IO, either by single injection or twice with a 12-h interval. All rats were sacrificed 12 or 24 h after the procedure, and mesenteric lymph nodes (MLN), liver, and blood samples were obtained under aseptic conditions for bacterial cultures. The samples were obtained 12 h following IO in the first two groups, and the same samples were obtained 24 h after IO in last three groups. Groups IV and V were the PTX treatment groups. PTX was re-injected 12 h after IO only in group IV. As a result, BT rates in MLNs and liver were found to be significantly low, blood specimens remained sterile in PTX-pretreated and -treated rats, and BT rates were high in control groups and group V (once treatment late specimen group). We conclude that simple intestinal obstruction causes BT, and PTX reduces BT in rats with IO during the first 12-h period if PTX is given once immediately following IO. PTX reduces BT during the first 24-h after IO provided that is injected twice with a 12-h interval. More experimental studies are need to explain the exact mechanism of this beneficial effect.

Analysis of Variance↗
PubMed1999

Bacterial translocation from the gastrointestinal tract.

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract to extraintestinal sites, such as the mesenteric lymph node complex (MLN), liver, spleen, kidney, and bloodstream. The three primary mechanisms promoting bacterial translocation in animal models are identified as: (a) disruption of the ecologic GI equilibrium to allow intestinal bacterial overgrowth, (b) increased permeability of the intestinal mucosal barrier, and (c) deficiencies in host immune defenses. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. In animal models in which the intestinal barrier is not physically damaged, indigenous bacteria translocate by an intracellular route through the epithelial cells lining the intestines and then travel via the lymph to the MLN. In animal models exhibiting damage to the mucosal epithelium, indigenous bacteria translocate intercellularly between the epithelial cells to directly access the blood. Indigenous GI bacteria have been cultured directly from the MLN of various types of patients. Thus, evidence is accumulating that translocation of indigenous bacteria from the GI tract is an important early step in the pathogenesis of opportunistic infections originating from the GI tract.

Animals↗
PubMed2000

Neutrophil depletion in rats reduces burn-injury induced intestinal bacterial translocation.

OBJECTIVE: To determine whether neutrophil depletion could eradicate intestinal bacterial translocation in bum-injured rats. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: The rats were intravenously administered a rabbit anti-rat neutrophil antibody causing profound neutropenia and subjected to a 30% total body surface area scald burn. MEASUREMENTS AND MAIN RESULTS: The depletion of neutrophils from the intestine was assessed via measurements of myeloperoxidase (MPO) activity in the intestinal homogenates. In addition, the presence of activated/extravasated neutrophils in intact intestines was determined via immunohistochemical localization of neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase component protein p47phox. Bacterial translocation was measured using agar cultures and by determining Escherichia coli beta-galactosidase gene via polymerase chain reaction/Southern blot analyses of mesenteric lymph node and spleen, liver, lung, and blood. MPO measurements demonstrated a six-fold increase above the control value in the intestinal tissue in rats on day 1 postburn. The presence of activated neutrophils (expression of p47phox protein) was also markedly increased in the intestines of these rats. The increased MPO activity and p47phox expression accompanied a translocation of indigenous E. coli into the mesenteric lymph node without a spread to other organs. The administration of anti-neutrophil antibody to burn animals prevented an increase in MPO activity and bacterial translocation. CONCLUSION: These studies indicate that enhanced intestinal bacterial translocation caused by burn injury could be related to the increased infiltration of activated neutrophils into the intestinal tissue after bum. The release of neutrophil products such as superoxide anion may effect intestinal tissue damage leading to bacterial translocation of indigenous E. coli.

Animals↗
PubMed2004

Study of bacterial translocation from gut after paraplegia caused by spinal cord injury in rats.

STUDY DESIGN: Normal rats and paraplegic rats with and injured spinal cord were used to study bacterial translocation from gut. OBJECTIVE: To investigate whether bacterial translocation from gut occurs after spinal cord injury. SUMMARY OF BACKGROUND DATA: It has been demonstrated that trauma and operation can lead to gastrointestinal paralysis; disturbance of gastrointestinal motility following trauma may cause bacterial overgrowth in gastrointestinal tract and increase the incidence of bacterial translocation. However, bacterial translocation from gut after spinal cord injury has not been studied. METHODS: Under aseptic manipulation, samples of blood were collected for bacterial cultures and endotoxin determination. In the meantime, samples of mesenteric lymph node, spleen, and liver were collected for bacterial culture. The jejunum and ileum were observed by light and electron microscope. RESULTS: Endotoxemia and bacterial translocation appeared 24 hours and 48 hours correspondingly after spinal cord injury complicated with paraplegia. CONCLUSION: Bacterial translocation from gut would occur after spinal cord injury in rats, which indicated that antibiotics should be administered to paraplegic patients with spinal cord injury as soon as possible to prevent potential bacterial translocation.

Animals↗
PubMed1996

The role of lactulose in the prevention of bacterial translocation in surgical trauma.

Surgical trauma (ST) is one of the causative factor of bacterial translocation. In this study we investigated the prevention of bacterial translocation with lactulose in a surgical trauma model. The study was designed in 3 experimental groups consisting of 15 rats in each. Group 1 was sham operated controls, group 2 was ST + physiologic saline treated and group 3 was ST + lactulose treated animals. Lactulose and physiologic saline were given by oro-gastric intubation in a dose of 2 ml of 33.5% solution/d and 2 ml/d respectively starting 3 days prior to surgery. Bacterial translocation was investigated 48 hours after the operations. In sham operated controls only 1 bacterial translocation to the mesenteric lymph nodes (MLN) was observed. In the ST + physiologic saline treated group bacterial translocation to the MLN and portal venous blood (PVB) were significantly increased compared with both sham operated controls and the ST + lactulose treated group (p < 0.001). In rats with lactulose treatment the results of caecal bacterial counts showed a significant decrease in the number of gram-negative aerobes and facultative anaerobe bacteria (p < 0.01) and a significant increase in the number of lactobacilli (p < 0.001) compared to the sham operated controls. Measurement of the mucosal height showed a significant increase at the terminal ileum and the caecum compared with the sham operated controls and the surgical trauma+physiologic saline treated group (p < 0.001). We conclude that oral lactulose treatment 3 days prior to the surgical trauma, reduced the incidence of bacterial translocation to the MLN and PVB.

Animals↗