Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal barrier”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed1990

Urinary excretion of differently sized polyethylene glycols after intravenous administration in uremic and control rats: effects of low- and high-protein diets.

The intestine constitutes a barrier towards potentially harmful agents in the intestinal lumen. Different-sized polyethylene glycols (PEGs; range 326-1,1162 Da) have been used to study the intestinal permeability properties in 5/6-nephrectomized rats on either a high- (22%) or low-protein (8%) diet. PEGs were administered intravenously, and the urinary recovery was measured. The 24-hour urinary recovery of PEGs was significantly reduced in the uremic groups. The ratios between different sizes of PEGs, indicating a size-selective escape of molecules from blood, were decreased in the uremic groups. The urinary recovery was in general increased in the control group on the high-protein diet compared to the control group on the low-protein diet. The results provide evidence for an increased permeability of larger PEGs (range 634-1,162 Da) in uremic rats and that the protein content of the diet might affect the permeability properties.

Animals↗
PubMed1999

Changes in gut mucosal nitric oxide synthase (NOS) activity after thermal injury and its relation with barrier failure.

This study was designed to investigate changes in mucosal NOS activity after burns and its relation to barrier failure. In Experiment 1, female specific pathogen free (SPF) Sprague-Dawley rats underwent 35% total body surface area (TBSA) burn. One to six days after burn, intestinal permeability was determined from the plasma leakage of fluorescein isothiocyanate (FITC)-dextran 4400, intestinal mucosal cNOS and iNOS activity were assayed using Griess' reagent, and the cellular localization of iNOS was examined using immunostaining. In Experiment 2, S-methylisothiourea (SMT) was given (5 mg/kg, i.p. every 12 h) for 2 days to suppress inducible NOS (iNOS) activity after thermal injury. On postburn Day 2, the effect of SMT on gut mucosal NOS activity, intestinal permeability, and barrier function were evaluated. The activity of iNOS increased 24 h after the injury and up to a maximum of twofold on postburn Day 2, and decreased thereafter. The increase in iNOS activity in gut mucosa correlated well with the increase in intestinal permeability, an index for barrier failure (r = .776, p = .0002). Results from iNOS immunostaining showed that changes in mucosal iNOS activity after the burn occurred mainly in the enterocytes rather than in the macrophages. Administration of SMT decreased mucosal iNOS activity, intestinal permeability, and bacterial translocation incidence to mesenteric lymph node concurrently. In conclusion, thermal injury induces intestinal mucosal iNOS, which is principally in the enterocytes. The increased intestinal iNOS activity was closely related to barrier failure. SMT inhibited intestinal mucosal iNOS activity and prevented barrier failure as demonstrated by a decrease in BT occurrence and intestinal permeability.

Animals↗
PubMed2005

Barriers to coliphage infection of commensal intestinal flora of laboratory mice.

BACKGROUND: Growth characteristics of coliphage viruses indicate that they are adapted to live with their Eschericia coli hosts in the intestinal tract. However, coliphage experimentally introduced by ingestion persist only transiently if at all in the gut of humans and other animals. This study attempted to identify the barriers to long term establishment of exogenous coliphage in the gastrointestinal (GI) tracts of laboratory mice. Intestinal contents were screened for the presence of coliphage and host bacteria, and strains of E. coli bacteria from different segments of the GI tract were tested for susceptibility to six common laboratory coliphages. RESULTS: Contrary to expectations, coliphage were not evident in the GI tracts of laboratory mice, although they were occasionally detected in feces. Commensal flora showed extreme variability within groups of mice despite identical handling and diet. Less than 20% of 48 mice tested carried E. coli in their gut, and of 22 commensal E. coli strains isolated and tested, 59% were completely resistant to infection by lambda, M13, P1, T4, T7, and PhiX174 coliphage. Lysogeny could not be demonstrated in the commensal strains as mitomycin C failed to induce detectable phage. Pre-existing immunity to phages was not evident as sera and fecal washes did not contain significant antibody titers to six laboratory phage types. CONCLUSION: Lack of sufficient susceptible host bacteria seems to be the most likely barrier to establishment of new coliphage infections in the mouse gut.

Animals↗
PubMed2002

Two msbB genes encoding maximal acylation of lipid A are required for invasive Shigella flexneri to mediate inflammatory rupture and destruction of the intestinal epithelium.

Shigella flexneri is a Gram-negative pathogen that invades and causes inflammatory destruction of the human colonic epithelium, thus leading to bloody diarrhea and dysentery. A type III secretion system that delivers effector proteins into target eukaryotic cells is largely responsible for cell and tissue invasion. However, the respective role of this invasive phenotype and of lipid A, the endotoxin of the Shigella LPS, in eliciting the inflammatory cascade that leads to rupture and destruction of the epithelial barrier, was unknown. We investigated whether genetic detoxification of lipid A would cause significant alteration in pathogenicity. We showed that S. flexneri has two functional msbB genes, one carried by the chromosome (msbB1) and the other by the virulence plasmid (msbB2), the products of which act in complement to produce full acyl-oxy-acylation of the myristate at the 3' position of the lipid A glucosamine disaccharide. A mutant in which both the msbB1 and msbB2 genes have been inactivated was impaired in its capacity to cause TNF-alpha production by human monocytes and to cause rupture and inflammatory destruction of the epithelial barrier in the rabbit ligated intestinal loop model of shigellosis, indicating that lipid A plays a significant role in aggravating inflammation that eventually destroys the intestinal barrier. In addition, neutralization of TNF-alpha during invasion by the wild-type strain strongly impaired its ability to cause rupture and inflammatory destruction of the epithelial lining, thus indicating that TNF-alpha is a major effector of epithelial destruction by Shigella.

Acylation↗
PubMed2000

Permeability of intestinal mucosa from urinary reservoirs in man and rat.

OBJECTIVE: To evaluate the barrier properties of intestinal mucosa chronically exposed to urine and to evaluate possible differences between ileal and colonic segments used in the reconstruction of the urinary tract. MATERIALS AND METHODS: Mucosal specimens from patients with continent reservoirs with an abdominal stoma, or orthotopic neobladders constructed from colonic segments, were obtained at revisional surgery. Control segments were obtained during right-sided hemicolectomy. In addition, ileal and colonic segments from enterocystoplasties in rats were assessed. The mucosa-to-serosa passage of marker molecules, i.e. (14)C-mannitol, (3)H-glucose, fluorescein isothiocyanate-dextran 4400 and ovalbumin, was measured using modified Ussing diffusion chambers. RESULTS: In man, there were no permeability differences between segments exposed to urine and control segments for any of the marker molecules. In rats, there was less passage of markers in ileal and colonic transplanted segments than in intestinal segments from sham-operated animals. CONCLUSIONS: Intestinal mucosa that has been in chronic contact with urine maintains its barrier function; in the rat model the permeability was even decreased. In addition, there were no detectable differences between ileal and colonic segments in this model.

Adult↗
PubMed2004

Functional and structural alterations of epithelial barrier properties of rat ileum following X-irradiation.

Irradiation of the digestive system leads to alterations of the small intestine. We have characterized the disruption of the barrier integrity in rat ileum from 1 to 14 days following irradiation ranging from 6 to 12 Gy. The intestinal permeability to 14C-mannitol and 3H-dextran 70 000 was measured in vitro in Ussing chambers. In parallel to these functional studies, immunohistochemical analyses of junctional proteins (ZO-1 and beta-catenin) of ileal epithelium were performed by confocal microscopy. Irradiation with 10 Gy induced a marked decrease in epithelial tissue resistance at three days and a fivefold increase in mannitol permeability, without modifications of dextran permeability. A disorganization of the localization for ZO-1 and beta-catenin was also observed. At 7 days after irradiation, we observed a recovery of the organization of junctional proteins in parallel to a return of intestinal permeability to control value. In addition to these time-dependent effects, a gradual effect on epithelial integrity of the radiation doses was observed 3 days after irradiation. This study shows a disruption of the integrity of the intestinal barrier in rat ileum following abdominal X-irradiation, depending on the time postirradiation and on the delivered dose. The loss of barrier integrity was characterized by a disorganization of proteins of tight and adherent junctions, leading to increased intestinal permeability to mannitol.

Animals↗
PubMed1993

Immunohistochemical study of tissue factor expression in normal intestine and idiopathic inflammatory bowel disease.

AIMS: To investigate the localisation of tissue factor expression in normal and inflamed intestine. METHODS: Serial cryostat sections of tissue taken from patients with Crohn's disease (n = 8), ulcerative colitis (n = 5), and from controls (n = 5) were stained with haematoxylin and eosin and immunostained for tissue factor, collagen type IV, fibrinogen and platelet glycoprotein IIIa. RESULTS: In control tissues tissue factor was present as a continuous layer along the epithelial basal lamina: sections from controls did not immunostain for fibrinogen or platelets. In non-ulcerated inflamed mucosa, tissue factor staining intensified in cases of Crohn's disease and was associated with fibrin deposition. Staining for tissue factor was either patchy or absent in cases of ulcerative colitis and there was no fibrin deposition. This change accompanied the early destruction of the epithelial basal lamina in ulcerative colitis that was not seen in Crohn's disease. In both diseases tissue factor expression in severely inflamed and ulcerated mucosa was present on lamina propria macrophages and vascular endothelium and was associated with fibrin or platelet thrombi. In three of eight cases of Crohn's disease tissue factor expression and thrombi were evident in areas of submucosal vasculitis. These were not seen in adjacent normal vessels. CONCLUSIONS: These observations are consistent with a tissue factor haemostatic barrier in the intestine: this barrier seems to be incomplete or defective in ulcerative colitis. Tissue factor expression by macrophages and endothelial cells may be important, particularly in the microvascular thrombosis and induration which are characteristic of Crohn's disease.

Adult↗
PubMed2003

PKC-beta1 isoform activation is required for EGF-induced NF-kappaB inactivation and IkappaBalpha stabilization and protection of F-actin assembly and barrier function in enterocyte monolayers.

Using monolayers of intestinal Caco-2 cells, we reported that activation of NF-kappaB is required for oxidative disruption and that EGF protects against this injury but the mechanism remains unclear. Activation of the PKC-beta1 isoform is key to monolayer barrier integrity. We hypothesized that EGF-induced activation of PKC-beta1 prevents oxidant-induced activation of NF-kappaB and the consequences of NF-kappaB activation, F-actin, and barrier dysfunction. We used wild-type (WT) and transfected cells. The latter were transfected with varying levels of cDNA to overexpress or underexpress PKC-beta1. Cells were pretreated with EGF or PKC modulators +/- oxidant. Pretreatment with EGF protected monolayers by increasing native PKC-beta1 activity, decreasing IkappaBalpha phosphorylation/degradation, suppressing NF-kappaB activation (p50/p65 subunit nuclear translocation/activity), enhancing stable actin (increased F-actin-to-G-actin ratio), increasing stability of actin cytoskeleton, and reducing barrier hyperpermeability. Cells stably overexpressing PKC-beta1 were protected by low, previously nonprotective doses of EGF or modulators. In these clones, we found enhanced IkappaBalpha stabilization, NF-kappaB inactivation, actin stability, and barrier function. Low doses of the modulators led to increases in PKC-beta1 in the particulate fractions, indicating activation. Stably inhibiting endogenous PKC-beta1 substantially prevented all measures of EGF's protection against NF-kappaB activation. We conclude that EGF-mediated protection against oxidant disruption of the intestinal barrier function requires PKC-beta1 activation and NF-kappaB suppression. The molecular event underlying this unique effect of PKC-beta1 involves inhibition of phosphorylation and increases in stabilization of IkappaBalpha. The ability to inhibit the dynamics of NF-kappaB/IkappaBalpha and F-actin disassembly is a novel mechanism not previously attributed to the classic subfamily of PKC isoforms.

Actins↗
PubMed2003

Epithelial transport and gut barrier function in colitis.

PURPOSE OF REVIEW: Colitis is an inflammatory bowel disease that is confined to the colon and is characterized by a watery diarrhea that can also be accompanied by blood in the stool. The inflammation associated with colitis is generally confined to the mucosal and submucosal layers, although Crohn's colitis may be transmural. The principal functions of the colonic mucosa are to act as a barrier to the luminal contents of the intestinal tract and to facilitate the bidirectional transport of water and electrolytes. It is well established that barrier and transport defects occur in colitis and may be involved in pathogenesis. Consequently, this review discusses recent evidence of potential mechanisms that may be involved in the perturbation of mucosal transport and barrier functions in colitis and therapeutic advances to counteract these defects. RECENT FINDINGS: Mechanisms responsible for transport dysfunction and barrier defects in colitis are discussed, including decreased activity of transport proteins such as CFTR, bacterial interactions with the epithelium, including understanding of the regulation and function of NOD-2, and altered expression of components of the intestinal barrier, such as mucins and multidrug resistance proteins. SUMMARY: Recent advances in our understanding of how changes in barrier and transport function occur in colitis may illuminate the pathophysiology of this condition. The work discussed may also identify novel targets that are functionally altered in colitis, which potentially can be modulated therapeutically either with existing medications or with newer agents that are in development.

Journal Article↗
PubMed1999

Intestinal cytokine response after gut ischemia: role of gut barrier failure.

OBJECTIVE: To investigate the effect of intestinal ischemia with and without a reperfusion injury on intestinal cytokine production and gut permeability. SUMMARY BACKGROUND DATA: In humans and in animal models, the gut has been implicated as a cytokine-producing organ after ischemia/reperfusion (I/R)-type injuries. Because of the limitations of in vivo models, it has been difficult to demonstrate directly that the gut releases cytokines after an I/R injury or whether there is a relation between the magnitude of the ischemic process and the cytokine response. METHODS: Ileal mucosal membranes from rats subjected to sham or 45 or 75 min of superior mesenteric occlusion (SMAO) or 45 minutes of SMAO and 30 minutes of reperfusion (SMAO 45/30) were mounted in the Ussing chamber system. Levels of tumor necrosis factor-alpha and interleukin-6 were serially measured in the mucosal and serosal reservoirs of the Ussing system, as was mucosal permeability as reflected by the passage of bacteria or phenol red across the ileal membrane. In a second group of experiments, Escherichia coli C25 was added to the mucosal reservoir to determine if the cytokine response would be increased. RESULTS: Mucosal and serosal levels of tumor necrosis factor-alpha were equally increased after SMAO, with the highest levels in the 75-minute SMAO group. The highest levels of interleukin-6 were found in rats subjected to 75 minutes of SMAO or SMAO 45/30; the serosal levels of interleukin-6 were four to sixfold higher than the mucosal levels. The addition of E. coli C25 resulted in a significant increase in the amount of interleukin-6 or tumor necrosis factor-alpha recovered from the mucosal reservoir. Increased ileal membrane permeability was observed only in rats subjected to 75 minutes of SMAO or SMAO 45/30. CONCLUSION: These results directly document that the levels of tumor necrosis factor-alpha and interleukin-6 released from the gut increase after an ischemic or I/R injury, such as SMAO, and that there is a relation between the magnitude of the gut ischemic or I/R insult and the cytokine response.

Animals↗
PubMed2007

Interleukin-6 induces keratin expression in intestinal epithelial cells: potential role of keratin-8 in interleukin-6-induced barrier function alterations.

Keratin 8 (K8) and keratin-18 (K18) are the major intermediate filament proteins in the intestinal epithelia. The regulation and function of keratin in the intestinal epithelia is largely unknown. In this study we addressed the role and regulation of K8 and K18 expression by interleukin 6 (IL-6). Caco2-BBE cell line and IL-6 null mice were used to study the effect of IL-6 on keratin expression. Keratin expression was studied by Northern blot, Western blot, and confocal microscopy. Paracellular permeability was assessed by apical-to-basal transport of a fluorescein isothiocyanate dextran probe (FD-4). K8 was silenced using the small interfering RNA approach. IL-6 significantly up-regulated mRNA and protein levels of K8 and K18. Confocal microscopy showed a reticular pattern of intracellular keratin localized to the subapical region after IL-6 treatment. IL-6 also induced serine phosphorylation of K8. IL-6 decreased paracellular flux of FD-4 compared with vehicle-treated monolayers. K8 silencing abolished the decrease in paracellular permeability induced by IL-6. Administration of dextran sodium sulfate (DSS) significantly increased intestinal permeability in IL-6-/- mice compared with wild type mice given DSS. Collectively, our data demonstrate that IL-6 regulates the colonic expression of K8 and K18, and K8/K18 mediates barrier protection by IL-6 under conditions where intestinal barrier is compromised. Thus, our data uncover a novel function of these abundant cytoskeletal proteins, which may have implications in intestinal disorders such as inflammatory bowel disease wherein barrier dysfunction underlies the inflammatory response.

Animals↗
PubMed1989

Is gastro-intestinal mucus an ion-selective barrier?

The mucus layer at the epithelial surface seems to be responsible for the formation of a microclimate in which the concentrations of H+, K+, Na+, and Cl- are rather constant. It is possible that this is not due simply to an unstirred layer effect, but also to a higher diffusion resistance of mucus. Flux measurements revealed that sodium and potassium permeabilities in mucus are 50% lower than those in saline. Dilution and biionic diffusion potentials indicated a higher relative permeability of mucus for sodium and potassium than for chloride. Thus mucus represents a diffusion barrier, slightly more permeable for cations than for anions.

Animals↗
PubMed1987

Aging-associated increase in intestinal permeability to polyethylene glycol 900.

Effect of aging on the intestinal permeability to medium size [3H]polyethylene glycol (PEG 900) was examined in vivo by gavage and in vitro in intestinal everted sacs of rats ranging in age from 5 to 102 weeks. Rats were gavaged with PEG 900 solution and urinary recovery of PEG 900 was measured for 6 hr in order to assess its absorption. Young rats, 5-15 weeks of age, absorbed 1-1.3% of administered PEG 900. In contrast, rats 35-102 weeks of age absorbed 1.8-2.4% of administered PEG 900 (P less than 0.05 vs younger animals). The increased absorption of PEG 900 with aging is due to changes in intestinal permeability since the total uptake (serosal appearance + tissue uptake) of PEG 900 by jejunum, ileum, and colonic everted sacs was significantly higher (P less than 0.05) in older rats (100 weeks) than young rats (9 1/2 weeks), while urinary excretion of PEG 900 following intravenous injection was the same in the two age groups. These studies indicate that aging rats have diminished capacity to exclude larger size molecules from penetrating the intestinal mucosa. The diminished barrier functions of the small intestine with aging may allow antigenic or mutagenic compounds to reach the systemic circulation.

Aging↗
PubMed2004

Relationship between protein deficiency in the ration of rats during early ontogeny and function of enzyme systems of digestive and non-digestive organs in adult life.

Low protein content in the ration of rat pups during transfer from mixed to definitive nutrition (days 21-30 of life) has a negative impact on digestive function of the small intestine and trophic and barrier functions of the large intestine, liver, and kidneys and increases (sucrase, glycyl-L-leucin dipeptidase) or decreases (alkaline phosphatase, aminopeptidase M, glycyl-L-leucine dipeptidase) enzyme activities in these organs in 6-month-old rats. Protein deficiency during the early ontogeny modulates functioning of the enzyme systems in digestive and non-digestive organs in adult life, which can lead to the development of not only gastrointestinal, but other visceral diseases.

Alkaline Phosphatase↗
PubMed2004

Surgical manipulation of the intestine results in quantitative and qualitative alterations in luminal Escherichia coli.

OBJECTIVES: To look at the qualitative and quantitative changes in the luminal bacterial flora in response to surgical manipulation of the small intestine. SUMMARY BACKGROUND DATA: The barrier function of the intestine is compromised in pathologic conditions, such as shock, trauma, or surgical stress. Our earlier work has shown that surgical manipulation results in oxidative stress in the intestinal mucosa leading to permeability alterations. METHODS: Studies were done on rats, which were randomly divided into four groups (n = 8): group I, control, group II, III, IV different time periods, such as 8, 12, and 24 hours after surgical manipulation, which was simulated by opening the abdominal wall and handling the intestine. The cecal wall and cecal luminal contents were harvested under sterile conditions and processed for quantitation for aerobes and anaerobes. Adherence assays using Hep-2 cells were carried out on Escherichia coli isolated under different experimental conditions. In addition, control E. coli were exposed to superoxide or hydrogen peroxide, followed by subculture and adherence studies. RESULTS: Surgical manipulation of the intestine resulted in qualitative and quantitative alterations in the aerobic bacteria. There was an increase in the number and relative proportion of E. coli in the cecal flora, and there was also an increase in adherence of E. coli to cecal mucosa, which was confirmed by in vitro bacterial adherence studies with HEp-2 cells. These changes were maximum at 12 hours following surgical manipulation and by 24 hours, this came back to control pattern. Control E. coli after in vitro exposure to oxidants also showed increased adherence. CONCLUSION: These studies suggest that oxidative stress in the mucosa following surgical manipulation results in alterations in the luminal bacteria leading to increased bacterial adherence onto mucosal epithelium, which may contribute to postsurgical complications.

Animals↗
PubMed2005

Transepithelial migration of Toxoplasma gondii involves an interaction of intercellular adhesion molecule 1 (ICAM-1) with the parasite adhesin MIC2.

Toxoplasma gondii crosses non-permissive biological barriers such as the intestine, the blood-brain barrier and the placenta thereby gaining access to tissues where it most commonly causes severe pathology. Herein we show that in the process of migration Toxoplasma initially concentrates around intercellular junctions and probably uses a paracellular pathway to transmigrate across biological barriers. Parasite transmigration required viable and actively motile parasites. Interestingly, the integrity of host cell barriers was not altered during parasite transmigration. As intercellular adhesion molecule 1 (ICAM-1) is upregulated on cellular barriers during Toxoplasma infection, we investigated the role of this receptor in parasite transmigration. Soluble human ICAM-1 and ICAM-1 antibodies inhibited transmigration of parasites across cellular barriers implicating this receptor in the process of transmigration. Furthermore, human ICAM-1 immunoprecipitated the mature form of the parasite adhesin MIC2 present on the parasite surface, indicating that this interaction may contribute to cellular migration. These findings reveal that Toxoplasma exploits the natural cell trafficking pathways in the host to cross cellular barriers and disseminate to deep tissues.

Animals↗
PubMed2002

Converting a peptide into a drug: strategies to improve stability and bioavailability.

The discovery of peptide hormones, growth factors and neuropeptides implicated in vital biological functions of our organism has increased interest in therapeutic use of short peptides. However, the development of peptides as clinically useful drugs is greatly limited by their poor metabolic stability and low bioavailability, which is due in part to their inability to readily cross membrane barriers such as the intestinal and blood-brain barriers. The aim of peptide medicinal chemistry is, therefore, to develop strategies to overcome these problems. Recent progress in chemical synthesis and design have resulted in several strategies for producing modified peptides and mimetics with lower susceptibility to proteolysis and improved bioavailability, which has increased the probability of obtaining useful drugs structurally related to parent peptides. This review describes different experimental approaches to transforming a peptide into a potential drug and provides examples of the usefulness of these strategies.

Biological Availability↗
PubMed2005

[Study on the mechanism of protective effect of oral L-arginine on intestine after scald injury in rats].

OBJECTIVE: To explore the mechanism of protective effect of oral L-arginine (L-Arg) on the intestine after scald injury in rats. METHODS: Sixty-six Sprague-Dawley (SD) rats were randomly divided into three groups: i.e. normal control (N, n = 6, without treatment), oral L-arginine group (A, n = 30, with 1 ml 70 g/L of L-Arg per os 2 times a day from 2 post scald hour (PSH)) on with normal enteral feeding and group B (n = 30, with oral feeding of cold boiled water after scald). The changes in the content of superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), endothelin (ET), ET/NO ratio in the intestine and the level of plasma endotoxin (LPS) in portal vein were assessed at 6, 12, 24, 48, 72 PSH. Ileum tissue samples were harvested for pathological examination. RESULTS: The ET content in the intestinal tissue in A group at 6, 12 and 24 PSH (0.80 +/- 0.26 ng/g, 0.75 +/- 0.30 ng/g, 0.63 +/- 0.22 ng/g) was obviously lower than that in B group (1.26 +/- 0.38 ng/g, 1.34 +/- 0.37 ng/g, 0.97 +/- 0.19 ng/g, P < 0.05), but the NO contents in the intestine in A group at the same time points were significantly higher than that in B group (P < 0.01). The ET/NO ratio and the level of plasma endotoxin in A group were significantly lower than those in B group at each time point (P < 0.05 or 0.01). Pathological examination showed that the intestinal mucosal injury in the A group was obviously milder than that in the B group. CONCLUSION: Oral L-arginine was shown to have the effects to ameliorate ischemia reperfusion injury of the intestine and to protect the barrier function of the intestinal mucosa. This might be related to an increase in the NO level in intestinal mucosa resulting in maintenance of a stable ET/NO ratio.

Animals↗