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PubMed2002

Comparison of effects of two hemoglobin-based O(2) carriers on intestinal integrity and microvascular leakage.

Two "blood substitutes," a diaspirin cross-linked human hemoglobin [bis(3,5 dibromosalicyl)fumarate, DBBF-Hb] and a bovine polymerized hemoglobin (PolyHbBv), advanced to clinical trials, are used in this study. Previously, we have shown that injection of DBBF-Hb into the rat circulation produces venular leakage and intestinal epithelial disruption. The purpose of this study was to determine whether PolyHbBv, currently approved for veterinary use in the United States, shows similar effects. In anesthetized Sprague-Dawley rats, the mesenteric microvasculature was perfused with DBBF-Hb (n = 6), PolyHbBv (n = 5), cyanomet Hb (CNmet-DBBF-Hb), or HEPES-buffered saline with 0.5% bovine serum albumin (HBS-BSA) (controls, n = 7) for 10 min, followed by FITC-albumin for 3 min, and then fixed for microscopy. For DBBF-Hb, the mean leak number per micrometer venule length [2.41 +/- 0.33 (+/-SE) x 10(-3)] was significantly greater than for PolyHbBv (0.53 +/- 0.14 x 10(-3)), CNmet-DBBF-Hb (0.36 +/- 0.14 x 10(-3)), and HBS-BSA (0.12 +/- 0.08 x 10(-3)) (P < 0.01). Corresponding quantities for leak area were 0.10 +/- 0.03, 0.010 +/- 0.003, 0.005 +/- 0.003, and 0.02 +/- 0.02 microm(2)/microm. In rats injected with DBBF-Hb (n = 8), intestinal epithelial integrity was significantly compromised compared with those injected with PolyHbBv (n = 5) or saline (n = 6). These results indicate that intravascular PolyHbBv produces significantly less disruption of the intestinal exchange barrier than does DBBF-Hb, probably because the heme is not so easily oxidized.

Animals↗
PubMed2005

Escherichia coli modulates extraintestinal spread of Staphylococcus aureus.

Staphylococcus aureus remains one of the most frequent causes of life-threatening systemic infection in surgical and trauma patients. It is understood that S. aureus colonization predisposes to complicating infection, but extraintestinal dissemination of S. aureus from the intestinal lumen to the draining mesenteric lymph nodes has not been systematically studied. After oral inoculation with high numbers of S. aureus, otherwise normal mice had low levels of cecal S. aureus (6.7 log10/g) and the incidence of extraintestinal dissemination was 30%. As expected, parenteral Escherichia coli lipopolysaccharide (LPS) was associated with increased numbers of cecal S. aureus, but the incidence of translocation remained unchanged. Purified LPS had no effect on S. aureus internalization by cultured HT-29 enterocytes and no effect on S. aureus transmigration through confluent enterocytes. To begin to clarify the effect of alterations in cecal bacteria on S. aureus translocation, mice were orally inoculated with E. coli and S. aureus. Compared with mice inoculated with S. aureus alone, these mice had increased numbers of cecal E. coli and S. aureus, and the incidence of S. aureus translocation nearly doubled from 46% to 88%. Experiments with HT-29 enterocytes indicated that viable E. coli had no effect on S. aureus internalization, but viable E. coli was at least 40 times more potent in inducing S. aureus transmigration across confluent enterocytes compared with a corresponding amount of purified LPS. Thus, S. aureus disseminated from the intestinal tract of normal mice by a mechanism that could involve paracellular migration across the intestinal epithelial barrier.

Animals↗
PubMed2004

Transcriptional downregulation of tight junction protein ZO-1 in active coeliac disease is reversed after a gluten-free diet.

UNLABELLED: Coeliac disease is an autoimmune enteropathy characterized by an enhanced permeability of the intestinal epithelial barrier. In epithelial cells paracellular permeability is regulated by intercellular tight junction. The cytoplasmic protein ZO-1 interacts directly with F-actin and plays a pivotal role in the structural and functional organization of tight junction. AIM: The aim of this study was to investigate the expression and localization of ZO-1 in the intestinal mucosa of coeliac patients. PATIENTS AND METHODS: Twenty patients with active coeliac disease, seven of whom underwent a repeat biopsy following a gluten-free diet and 27 control subjects, were studied. In all subjects, three biopsies were obtained from distal duodenum during upper gastrointestinal endoscopy. ZO-1 protein localization and levels were detected by immunofluorescence followed by confocal microscopy analysis and immunoblotting. ZO-1 mRNA expression was assessed by RT-PCR. F-actin distribution was also investigated. RESULTS: In patients with active coeliac disease, both ZO-1 protein levels and mRNA were clearly reduced. Cytoskeletal organization was disrupted with F-actin staining concentrated at the subcortical and basal surface regions. Abnormalities in ZO-1 expression and actin organization were reversed after a gluten-free diet. CONCLUSIONS: In active coeliac disease, ZO-1 protein expression is downregulated at the transcriptional level in association with F-actin redistribution. These changes are completely reversed after a gluten-free diet and could contribute to the increased intestinal paracellular permeability observed in this disorder.

Actins↗
PubMed2003

Chronic fatigue syndrome: lactic acid bacteria may be of therapeutic value.

Chronic fatigue syndrome (CFS) is complex illness with unknown aetiology. Recent research shows that patients with CFS have marked alterations in microbial flora, including lowered levels of bifidobacteria and small intestinal bacterial overgrowth (SIBO). Research also indicates that CFS patients are under increased oxidative stress, have a type 2 helper cell dominate cytokine profile, frequently report allergies, have altered essential fatty acid (EFA) status and may have malabsorption of certain micronutrients. Lactic acid bacteria (LAB) have the potential to influence the immune system in CFS patients by supporting T helper cell 1 driven cellular immunity and may decrease allergies. In addition LAB are strong antioxidants, may improve EFA status, can enhance absorption of micronutrients by protecting the intestinal epithelial barrier, and have been used to treat SIBO. It is our contention that LAB may have a therapeutic role in the treatment of CFS.

Cytokines↗
PubMed1991

Bacterial translocation.

The phenomenon of bacterial translocation, the movement of viable indigenous microorganisms across the intestinal epithelial barrier, has been recognized for almost 100 years. At the present time, the precise mechanism of microbial transport is unknown. Active epithelial uptake and phagocyte-mediated transport have been proposed as likely explanations for the extraintestinal movement of bacteria to mesenteric lymph nodes and distant organ sites. Translocation has been proposed as the pivotal process associated with intestinal origin portal sepsis in seriously ill and immunocompromised patients. While several etiologic factors can be implicated in the pathogenesis of bacterial translocation, the present clinical implications are based almost solely on studies of dogs, rats and mice. Present investigations continue to suggest a causal relationship between intestinal mucosal integrity and infection by indigenous gastrointestinal bacteria.

Animals↗
PubMed2003

Probiotics: what are they? What are their effects on gut physiology?

Probiotics can be defined as microbial cells that have a beneficial effect on the health and well-being of the host. Since the gastrointestinal mucosa is the surface of contact with probiotics, it seems evident that the first effects of probiotics relate to digestive function. A brief review of the literature indicates that probiotics have very few effects on the main physiological functions of the gastrointestinal tract, which are digestion, absorption and propulsion. The main action of probiotics can be summarised as a reinforcement of the intestinal mucosal barrier against deleterious agents. Experimental data indicate that some probiotics reduce pathological alterations in paracellular permeability to large molecules or bacteria, stimulate mucosal immunity, display a trophic action on the mucosa, reduce mucus degradation and interact with mediators of inflammation. Yoghurt may help lactose digestion, and some data needing confirmation indicate a stimulation of water absorption and an acceleration of intestinal transit by some bacteria.

Animals↗
PubMed2000

Platelet-activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E-cadherin.

1. Platelet-activating factor (PAF), an inflammatory mediator, plays an important role in mediating intestinal injury. However, it remains unclear whether PAF has a function in the intestine. The production of PAF by normal intestine and by unstimulated intestinal epithelial cell lines suggests that PAF may have a regulatory function in the normal bowel. 2. In this study we investigated the role of PAF in modulating intestinal mucosal permeability in rats. Lumen-to-blood transit of FD-4 (dextran 4400), (an index of intestinal permeability), was assessed in sham-operated rats and rats injected with PAF (1.25 microg kg(-1), i.v., a dose insufficient to induce intestinal injury). 3. PAF-induced villus cytoskeletal changes were examined by staining the intestine for F-actin. The effect of PAF on tyrosine phosphorylation of the junctional protein E-cadherin was examined by immunoprecipitation. Some rats were pretreated with AG1288 (a tyrosine kinase inhibitor) before PAF injection, and mucosal permeability change was assessed. 4. To investigate the role of endogenous PAF upon mucosal permeability, we studied the effect of PAF antagonists on (intraluminal) glucose-induced increase in mucosal permeability. 5. We found that low dose PAF: (a) alters the cytoskeletal structure of intestinal epithelium, (b) causes the influx of FD4 from intestinal lumen to systemic circulation, (c) induces tyrosine phosphorylation of E-cadherin and cadherin-associated proteins. Glucose-induced mucosal permeability increase is abolished by using two structurally different PAF antagonists. 6. These results suggest that endogenous PAF modulates macromolecular movement across the intestinal mucosal barrier, probably via tyrosine phosphorylation of E-cadherin and cytoskeletal alteration of enterocytes.

Animals↗
PubMed2001

[Therapeutic drug monitoring of immunosuppresants].

The pharmacokinetics and pharmacodynamics of tacrolimus were evaluated in the pediatric recipients of living-related liver transplant. The mean clearance for tacrolimus was estimated with large interindividual variability and was shown to change as a function of days after operation. The therapeutic blood concentration of tacrolimus ranges were concerned from nearly 10 to 20 ng/ml. We have examined whether the expression levels of the intestinal absorptive barriers, MDR1 gene product P-glycoprotein and cytochrome P450 IIIA4(CYP3A4), correlate with the trough levels of orally administered tacrolimus in a recipient of small bowel transplant for 4 months. Both the MDR1 and CYP3A4 mRNA levels changed markedly through out this period. The tacrolimus concentration/dose ratio correlated well with the mRNA expression level of MDR1, but not CYP3A4. Intestinal P-glycoprotein rather than CYP3A4 is a good probe to predict the intraindividual variation in the tacrolimus pharmacokinetics.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Alterations in intestinal fatty acid metabolism in inflammatory bowel disease.

Inflammatory bowel disease (IBD) constitutes a severe intestinal disorder in developed countries with increasing incidence worldwide. Upcoming evidence indicates an important role of intestinal epithelial barrier function in the development of IBD. Fatty acids exert nutritional and protective effects on enterocytes, serve as activators of transcription and constitute precursors of inflammatory mediators. The aim of this study was to investigate differential regulation of genes involved in fatty acid uptake and endogenous fatty acid biosynthesis in IBD. Mucosal biopsy specimens from non-affected regions of the intestine were subjected to DNA microarray analysis. Gene array analysis revealed a variety of genes involved in fatty acid uptake and synthesis to be differentially expressed in ileum and colon of selected IBD patients. To verify these results, real-time RT-PCR was performed for selected regulated candidate genes in larger IBD sample numbers. In single biopsy analysis long chain acyl-CoA synthetase (ACSL) 1 and 4 were upregulated in IBD (P<0.05), while a significant decrease in fatty acid synthase expression was found in ileum and colon of ulcerative colitis patients (P<0.001). Expression of the transcription factor liver X receptor (LXR) which was previously shown to induce fatty acid synthase gene expression was not altered on mRNA level in IBD. However, in cell culture experiments using the human intestinal cell line LS174T induction of fatty acid synthase by the LXR ligand T0901317 was inhibited by TNFalpha. Moreover, these experiments indicated a decrease of LXR protein levels by TNFalpha treatment. These data suggest that the decrease of fatty acid synthase expression in ulcerative colitis patients could be at least partially due to a loss of LXR expression and function in the presence of pro-inflammatory cytokines. Observed alterations in expression of genes of fatty acid metabolism may contribute to the pathophysiology of ulcerative colitis.

Animals↗
PubMed2002

A gnotobiotic transgenic mouse model for studying interactions between small intestinal enterocytes and intraepithelial lymphocytes.

The mouse intestinal epithelium undergoes continuous renewal throughout life. Intraepithelial lymphocytes (IELs) represent a significant fraction of this epithelium and play an important role in intestinal mucosal barrier function. We have generated a germ-free transgenic mouse model to examine the effects of a genetically engineered proliferative abnormality in the principal epithelial cell lineage (enterocytes) on IEL census and on IEL-enterocytic cross-talk. SV40 large T antigen (TAg(Wt)) or a mutant derivative (TAg(K107/8)) that does not bind pRB was expressed in small intestinal villus enterocytes under the control of elements from the intestinal fatty acid binding protein gene (Fabpi). Quantitative immunohistochemical and flow cytometric analyses of conventionally raised and germ-free FVB/N Fabpi-TAg(Wt), Fabpi-TAg(K107/8), and nontransgenic mice disclosed that forced reentry of enterocytes into the cell cycle is accompanied by an influx of thymically educated alphabeta T cell receptor (TCR)(+) CD4(+) and alphabeta TCR(+) CD8alphabeta(+) IELs and a decrease in intestinally derived gammadelta TCR(+) CD8alphaalpha IELs. Real time quantitative reverse transcriptase-PCR studies of jejunal villus epithelium recovered from germ-free transgenic and normal mice by laser capture microdissection and gammadelta TCR(+) jejunal IELs purified by flow cytometry disclosed that the proliferative abnormality is accompanied by decreased expression of enterocytic interleukin-7 as well as IEL interleukin-7Ralpha and transforming growth factor beta3. The analysis also revealed that normal villus epithelium expresses Fms-like tyrosine kinase 3 (Flt3), a known regulator of hematopoietic stem cell proliferation and neuronal cell survival, and its ligand (Flt3L). Epithelial expression of this receptor and its ligand is reduced by the proliferative abnormality, whereas IEL expression of Flt3L remains constant. Together, these findings demonstrate that changes in the proliferative status of the intestinal epithelium affects maturation of gammadelta TCR(+) IELs and produces an influx of alphabeta TCR(+) IELs even in the absence of a microflora.

Animals↗
PubMed2001

Effects of early enteral feeding on the prevention of enterogenic infection in severely burned patients.

The aim of the study was to analyse the effects of early enteral feeding on the prevention of enterogenic infection in severely burned patients. A total of 22 patients with severe burns were randomly divided into an early enteral feeding group (EF) and a delayed enteral feeding group (DF). The levels of serum endotoxin and TNF-alpha were dynamically detected in the members of both groups, and two unmetabolized sugars (lactulose and mannitol) were orally administered to these patients 1, 3 and 5 days postburn. Intestinal permeability was evaluated by detecting the concentrations of lactulose and mannitol in the urine and the lactulose-mannitol ratio (L/M) ratio. The levels of serum endotoxin and TNF-alpha in severely burned patients were significantly higher than in normal subjects (P<0.01). The endotoxin level was positively related to the TNF-alpha level (rEF=0.93, P<0.01; rDF=0.80, P<0.05). The urinary lactulose levels in both groups were significantly higher than in normal (P<0.01), the urinary mannitol levels showed no obvious changes (P>0.05). The urinary L/M ratios in both groups were significantly higher than in normal subjects (P<0.01). The urinary L/M ratio was positively related to the serum endotoxin level (r=0.95, P<0.01). The urinary lactulose levels and the urinary L/M ratios in the EF group were significantly lower than in the DF group (P<0.01). The levels of serum endotoxin and TNF-alpha in the EF group were significantly lower than in the DF group (P<0.01). It is suggested that intestinal permeability was markedly higher after burns than normal, and was positively related to the gut-derived endotoxemia. Early enteral feeding may decrease intestinal permeability, preserve the intestinal mucosal barrier and have a beneficial effect on the reduction of enterogenic infection.

Adolescent↗
PubMed1991

Supraphysiologic L-tryptophan elicits cytoskeletal and macromolecular permeability alterations in hamster small intestinal epithelium in vitro.

We have previously shown that Na(+)-coupled transport of glucose and amino acids across the apical membrane of intestinal absorptive cells is accompanied by alterations in cytoskeletal structure and altered sieving of small hydrophilic solutes by tight junctions. Here we report that in response to the essential amino acid L-tryptophan at lumenal concentrations likely to be supraphysiological (1 mM or greater), these responses are so exaggerated as to induce disruption of tight junctions and transepithelial macromolecular leaks. Since these effects of L-tryptophan are energy and Na+ dependent and occur with mucosal but not serosal exposure to L-tryptophan, it appears they are triggered by activation of a Na(+)-nutrient cotransporter in the apical membrane of absorptive cells rather than by the presence of an unidentified trace contaminant. Our findings suggest the possibility that dietary supplementation by L-tryptophan may result in loss of the intestinal epithelial barrier to dietary antigens. We speculate that such a response to supraphysiologic tryptophan may contribute, in part, to the recently recognized curious tryptophan-induced eosinophilia myalgia syndrome.

Animals↗
PubMed2006

Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis.

A small percentage of pathologically obese subjects with fatty livers develop histological signs of necroinflammation and fibrosis, suggesting a variety of cofactors in the pathogenesis of obesity-related liver diseases including nonalcoholic steatohepatitis. Since several observations have linked bacterial endotoxins to liver damage, the aim of this study was to determine the effect of obesity on intestinal mucosal integrity and portal blood endotoxemia in two strains of obese mice: leptin-deficient (ob/ob) and hyperleptinemic (db/db) mice. Murine intestinal mucosal barrier function was assessed using a Ussing chamber, whereas ileum tight junction proteins were analyzed by immunocytochemistry and Western blot analysis. Circulating proinflammatory cytokines and portal blood endotoxin levels were measured by ELISA and the limulus test, respectively. The inflammatory and fibrogenic phenotype of murine hepatic stellate cells (HSCs) was determined by ELISA and quantitative RT-PCR. Ob/ob and db/db mice showed lower intestinal resistance, profoundly modified distribution of occludin and zonula occludens-1 in the intestinal mucosa, and higher circulating levels of inflammatory cytokines and portal endotoxemia compared with lean control mice. Moreover, HSCs isolated from ob/ob and db/db mice showed higher membrane CD14 mRNA levels and more pronounced lipopolysaccharide-induced proinflammatory and fibrogenic responses than HSCs from lean animals. In conclusion, genetically obese mice display enhanced intestinal permeability leading to increased portal endotoxemia that makes HSCs more sensitive to bacterial endotoxins. We suggest that in metabolic syndrome, patients may likewise have a greater intestinal mucosa permeability and increased lipopolysaccharide levels in portal blood that can contribute to the liver inflammatory damage.

Animals↗
PubMed1997

Effect of glutamine or glucagon-insulin enriched total parenteral nutrition on liver and gut in 70% hepatectomized rats with colon stenosis.

BACKGROUND: Malnutrition of enterocytes is believed to facilitate the breakdown of the intestinal mucosal barrier, furthering a translocation of enteric bacteria with subsequent severe infection, which has been described after extensive hepatectomy. Glutamine and glucagon insulin are said to attenuate the malnutrition of enterocytes. To determine whether this was true, the effects on the remnant liver and the gut of total parenteral nutrition supplemented by admixtures of glutamine and/or glucagon insulin were investigated in rats subjected to massive hepatectomy and transient intestinal stasis. STUDY DESIGN: Rats underwent a permanent cannulation of the superior caval vein without restraining their mobility, a 70% hepatectomy, and a 24 hour string-ligation stenosis of the colon. A standard total parenteral nutrition solution was infused without or with 2% glutamine and without or with glucagon-insulin supplementation, respectively. RESULTS: Glutamine and glucagon-insulin supplemented total parenteral nutrition increased ileal mucosal DNA concentrations during and after intestinal stasis. Glutamine or glucagon-insulin alone had less pronounced effects. In the liver, the combined supplementation resulted in reduced adenosine triphosphate concentrations and increased mitochondrial adenosine triphosphate synthesis as well as in an early increase in DNA concentrations. CONCLUSION: Glutamine and glucagon-insulin enriched total parenteral nutrition attenuates malnutrition of enterocytes after massive abdominal stress and promotes liver regeneration after extensive hepatectomy.

Alanine Transaminase↗
PubMed2004

[Analysis of the therapeutic effect and the safety of glutamine granules per os in patients with severe burns and trauma].

OBJECTIVE: To observe the therapeutic effect and possible side effects of glutamine granules per os in patients with trauma, burns and major operations. METHODS: Patients inflicted with severe burns, trauma and major operations were enrolled in the study. One hundred and twenty patients were randomly divided into two groups, 60 in control group (C) and 60 in glutamine group (Gln). Randomized double blind and placebo control methods were employed in the study. All the patients in both groups were given diet with equal calories and equal nitrogen content. The patients in Gln group received glutamine granules in dose of 0.5 g.kg(-1).d(-1) orally or by gavage, while those in C group received same dose of placebo (glycine) for 7 days. The changes in the intestinal mucosal barrier function, the protein metabolism, the immune function, hepatic and renal functions, and the incidence of side effects of the medication in both groups of patients were observed and compared before and after the supplementation of glutamine or glycine. RESULTS: The plasma contents of glutamine, proteins and interleukin 2 in both groups were all lower than normal values. But the plasma diamine oxidase (DAO) activity, endotoxin content, intestinal mucosal permeability (urine lactose/mannitol, L/M) and urine excretion of nitrogen increased obviously in both groups. The plasma glutamine concentration in Gln group increased by 38.04% after the administration of Gln for 7 days (P < 0.01). The plasma contents of pro-albumin, transferrin, and IL-2 were obviously higher than those in the C group (the increase rates were 21.19%, 51.11%, 57.54%, respectively, P < 0.01). The plasma DAO activity, L/M ratio, endotoxin content and urine nitrogen excretion in Gln group were evidently lower than those in C group (the decrease rates were 47.26%, 52.18, 22.22% and 27.78%, respectively, P < 0.05 or 0.01). There was no obvious difference in the plasma levels of total protein and albumin, the indices in blood and urine test, or the hepatic and renal functions between the two groups before and after the amino acid supplementation. Mild side effects such as nausea, diarrhea, constipation occurred in both groups, but all of them disappeared spontaneously afterwards (P > 0.05). CONCLUSION: Oral administration of glutamine could be helpful to increase plasma concentration of glutamine and to ameliorate obviously the intestinal mucosal injury, to promote systemic protein synthesis and to inhibit protein catabolism and to upgrade systemic immune function with little side effect in patients with severe injury.

Administration, Oral↗
PubMed2000

Ileal mucosal response to bacterial toxin challenge.

BACKGROUND: The cause of postinjury intestinal mucosal barrier disruption remains obscure. The present study examines the hypothesis that the bacterial toxin formyl-methionyl leucyl phenylalanine (FMLP) plays an initial role in this process. METHODS: Mucosal permeability to fluorescein isothiocyanate-labeled dextran (4,400 molecular weight) was measured in perfused distal rat ileum with and without FMLP. Dextran and myeloperoxidase appearance in the lumenal perfusate was assessed in response to surrogates of traumatic stress: ischemia/reperfusion, total abdominal irradiation, and total parenteral nutrition. Recovery of FMLP in the effluent of static closed and perfused ileal loops was determined by mass spectrometry. Release of mast cell mediators in the presence of FMLP was determined in ileal everted sacs. RESULTS: Seventy-five percent of FMLP was recovered in perfusion effluent in contrast to 5% in closed loops. There was a transient increase in ileal permeability in FMLP/perfused, untreated rats, and in ischemia/reperfusion and total parenteral nutrition treated rats that was recorded with a concomitant increment in myeloperoxidase (inflammatory marker) in all experimental models except irradiated rats, which were unresponsive to FMLP. FMLP responsiveness was associ. ated with a significant rise in release of serotonin (mast cell mediator). CONCLUSION: These results suggest that mast cells and other resident inflammatory cells within the gut wall are involved in FMLP-induced changes in mucosal barrier permeability and raise the possibility that under conditions of traumatic stress, proinflammatory mediators within the gut wall might be activated by toxic factors in the gut lumen.

Animals↗
PubMed2005

Intestinal microflora in rats with ischemia/reperfusion liver injury.

OBJECTIVES: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. METHODS: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial count, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. RESULTS: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in I/R group compared to those in the sham group. Intestinal Bifidobacterium and Lactobacillus decreased and intestinal Enterobacteria and Enterococci, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group. CONCLUSION: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, which contributes to endotoxemia and bacterial translocation to kidney.

Animals↗
PubMed1976

Spontaneous bacterial peritonitis induced by intraarterial vasopressin therapy.

Two patients developed spontaneous bacterial peritonitis after infusions of vasopressin into the superior mesenteric or gastroduodenal arteries for upper gastrointestinal hemorrhage. The peritonitis in these patients differed from the typical picture in which a single aerobic organism is responsible, by the presence of multiple organisms, some of which were anaerobic. These findings suggest that the arterial vasoconstriction decreased the integrity of the intestinal mucosal barrier and permitted the transmural migration of enteric organisms from the lumen of the bowel into the ascites-filled peritoneal cavity.

Anaerobiosis↗