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PubMedDate not supplied

Evidence of secondary neuronal intestinal dysplasia in a rat model of chronic intestinal obstruction.

The etiology of neuronal intestinal dysplasia remains largely unknown. There is, however, supporting evidence of the existence of Hirschprung's disease or chronic intestinal obstruction associated with neuronal intestinal dysplasia. With the aim of investigating the possible development of neuronal intestinal dysplasia linked to chronic intestinal obstruction, we have examined the enteric nervous system response to long-term obstruction in a rat model. Three different surgical techniques were tested in Wistar male rats. In animals that survived longer than the cutoff chronic intestinal obstruction point (6 weeks), full-thickness biopsies and acetylcholinesterase (AChE), NADH, hematoxylin-eosin, and anti-S100 protein stainings were performed. The results of our model indicate that chronic intestinal obstruction induced different degrees of enteric nervous system dysplasia, including histological features of neuronal intestinal dysplasia. The relationship between chronic intestinal obstruction and anomalies of the enteric nervous system, including neuronal intestinal dysplasia, needs to be further studied.

Acetylcholinesterase↗
PubMed2006

[Anatomic study of small intestinal vessel in piglet small intestine transplantation].

OBJECTIVE: To study the anatomy of the small intestine,and investigate the optimal selection of donors,recipients,and their small intestine vessels in piglet small intestine transplantation. METHODS: The weight and length of 30 piglets were measured. Angiography and pigments perfusion were used to observe the main vessels of the small intestine,and the length of the small intestine,and the external diameter of the main vessels of the small intestine were measured in vivo and ex vivo. RESULTS: The length of the small intestine was 11.5 times as long as the body length, and its weight accounted for 2.3% of the body weight. The outer diameters of abdominal aorta (AT), mesenteric anterior artery (MAA) and its 5(th)-6(th) branches in vivo and ex vitro were 4.3/4.6mm, 2.5/2.7mm and 1.9/2.2mm respectively. The total number of MAA's branches was 6-8 in general and its 5(th)-6(th) branches were the longest [(20.0 +/- 7.0) mm, (22.0 +/- 8.2) mm]. The outer diameter of mesenterial anterior vein (MAV) was 1-2 mm wider than that of MAA. CONCLUSIONS: AT, MAA and its 5(th)-6(th) branches are the preferable vessels for small intestine transplantation. In segmental small intestine transplantation, the length of the small intestine and body weight can be used to primarily select the suitable animals.

Animals↗
PubMedDate not supplied

First-pass metabolism of gentisamide: influence of intestinal metabolism on hepatic formation of conjugates. Studies in the once-through vascularly perfused rat intestine-liver preparation.

Gentisamide (GAM) metabolism was studied in a once-through in situ perfused rat intestine-liver preparation in a manner which mimicked the first-pass effect. GAM (2.56 to 392 microM) was delivered into the intestine via the superior mesenteric artery at a flow of 7.5 ml/min. The intestinal venous outflow into the portal vein and the hepatic arterial flow (2.5 ml/min; without drug) served as dual inflows into the liver. The steady state intestinal extraction ratios (E1, 0.33 to 0.06) and hepatic extraction ratios (EH, 0.84 to 0.37) were highly concentration dependent, decreasing with increasing GAM concentrations. Gentisamide-5-glucuronide was found to be the major intestinal metabolite, and gentisamide-2-sulfate was also formed, albeit to a much lesser extent. However, hepatic metabolism of GAM revealed 5-sulfation and glucuronidation as the predominant pathways, with GAM 2-sulfation as a minor pathway. About 1 to 3% and 7% of dose was excreted into lumen and bile, respectively, mostly as GAM-5G. From the metabolic data, the fitted parameters confirmed that more enzymes exist in the liver than in intestine for the processing of GAM. The Km for 2-sulfation by the intestine was higher than the apparent Kms observed for 2- and 5-sulfation in liver. However, the Kms for 5-glucuronidation for both the intestine and liver were similar. The interrelationship between intestine and liver formation of first-pass metabolites showed that, at low GAM input concentration entering the IL preparation, the intestine, being the anterior organ, regulated the available substrate for hepatic elimination, and hence reduced the contribution of hepatic metabolism in the overall first-pass effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Route of lymphocyte migration in pigs. II. Migration to the intestinal lamina propria of antigen-specific cells generated in response to intestinal immunization in the pig.

Intestinal lymph-duct cannulae were established in normal and mesenteric lymphadenectomized (MLNx) pigs for the 6-day duration of a local intestinal immune response to a protein antigen (ovalbumin). The daily output of anti-ovalbumin-containing cells (AOCC) in intestinal lymph and the numbers of AOCC in the intestinal lamina propria at the end of the experiment were recorded. Very few AOCC were recovered in the intestinal lymph of normal pigs whereas in MLNx pigs large numbers were recovered reaching a peak output on day 4. However, there were significantly more AOCC detected in the jejunal lamina propria of normal pigs than MLNx pigs despite continuous drainage of intestinal lymph throughout the response. The absence of AOCC from efferent intestinal lymph of normal pigs, the failure of chronic intestinal-lymph drainage to abrogate the AOCC response in the intestine of these pigs and the reversal of these findings in MLNx pigs indicate that, in contrast to other species, lymphoblasts are diverted from porcine intestinal lymph, and probably enter the blood circulation at the level of the mesenteric lymph node (MLN).

Animals↗
PubMed1997

Concurrent overexpression of cyclin D1 and cyclin-dependent kinase 4 (Cdk4) in intestinal adenomas from multiple intestinal neoplasia (Min) mice and human familial adenomatous polyposis patients.

We postulated that increased expression of the cell cycle regulators cyclin D1 and cyclin-dependent kinase (Cdk) 4 may be involved in the development of intestinal adenomas associated with familial adenomatous polyposis (FAP). In the present study of multiple intestinal neoplasia (Min) mice and human FAP patients, the expression and distribution of cyclin D1, Cdk4, and cell proliferative activity (5-bromo-2'-deoxyuridine incorporation) in normal and adenomatous intestinal epithelium were investigated. Immunohistochemical analysis of Min mouse intestine revealed that cyclin D1 immunoreactivity in the intestinal epithelium was restricted to the adenomatous areas, with a significantly higher percentage of positively staining nuclei in high-grade dysplasia versus low-grade dysplasia (54.8 +/- 18.4% versus 34.6 +/- 16.9%, P = 0.016). Morphologically normal areas of intestinal epithelia were uniformly negative for cyclin D1 immunoreactivity. Cdk4 nuclear immunoreactivity was restricted to the crypt areas in morphologically normal small intestine and colon. Conversely, Cdk4 immunoreactivity was uniformly abundant in adenomatous areas regardless of the degree of dysplasia. Increased expression of cyclin D1 and Cdk4 in adenomas was accompanied by a significantly increased 5-bromo-2'-deoxyuridine incorporation rate in the same areas. Immunoblot analysis of lysates from surgical specimens revealed increased levels of cyclin D1 and Cdk4 in the majority of intestinal adenomas from human FAP patients in comparison to the adjacent grossly normal colonic mucosa. Our results indicate that overexpression of cyclin D1 and Cdk4 occurs in intestinal adenomas and is associated with increased cell proliferative activity in premalignant neoplastic cells. Increased cyclin D1 immunoreactivity is associated with more severe dysplasia. These data suggest that abnormal up-regulation of these important G1 cell cycle proteins is a relatively early event in intestinal carcinogenesis and that these changes may contribute to malignant progression within those lesions.

Adenomatous Polyposis Coli↗
PubMed1996

[Intestinal cytokine liberation after intestinal ischemia in the rat--studies in the Ussing chamber system].

UNLABELLED: Intestinal ischemia, frequently found in clinical states such as aortic bypass operations or hemorrhagic shock, is associated with loss of gut barrier function. Subsequent translocation of indigenous bacteria and endotoxin have been implicated as a major contributor to a systemic immuno-inflammatory response, which finally leads to multiple organ failure. There is increasing evidence that intestinal injury can result in the gut becoming a cytokine generating organ. This study was designed to show direct evidence of the gut as a major source of proinflammatory cytokines after intestinal ischemia and to further relate this cytokine response to the extent of intestinal ischemia/reperfusion. Additionally the potential role of the altered intestinal barrier function after intestinal ischemia for this cytokine response was investigated. METHODS: Rats were subjected to occlusion of the superior mesenteric artery for 45 min. (SMAO45), 75 min. (SMAO75), SMAO for 45 min. and 30 min. reperfusion (SMAO45/30), or sham SMAO, and then killed. Mucosal membranes from the terminal ileum were mounted in a Ussing chamber. E. coli C25 was added to the mucosal side of the stripped gut epithelium in half of the chambers. TNF and IL-6 levels on mucosal and serosal side of the stripped gut epithelium were assessed serially over 3 hrs. Gut barrier function was assessed by in vitro bacterial translocation (BT) and the transepithelial resistance (TER) of the mucosal membrane. RESULTS: The TNF response was greatest in the SMAO75 group, the IL-6 response in the SMAO75 and SMAO45/30 groups. In the absence of E. coli C25. IL-6 was produced to a greater extent on the serosal side, while addition of bacteria led to a significantly increased TNF/IL-6 response at the mucosal side of the stripped gut epithelium. BT was increased in SMAO75 and SMAO45/30 rats. Baseline TER was decreased in all experimental compared to sham SMAO groups. Although gut barrier function was impaired after intestinal ischemia/reperfusion there was no correlation between intestinal cytokine response and gut permeability. CONCLUSIONS: The gut becomes a cytokine liberating organ alter intestinal ischemia/reperfusion. This cytokine response is affected by certain conditions, but is not directly related to an impaired intestinal barrier function.

Animals↗
PubMed1981

Vasoactive intestinal polypeptide (VIP)-like immunoreactivity in anuran intestine.

Immunocytochemical and radioimmunological techniques with region specific antisera have been used to identify a vasoactive intestinal polypeptide-like material in the anuran intestine. Seven species of Anura were investigated: Bombina bombina, Alytes obstetricans, Rana temporaria, Rana esculenta, Hyla arborea, Hyla crepitans and Bufo bufo. In five of the species (A. obstetricans, R. temporaria, H. arborea, H. crepitans and B. bufo) vasoactive intestinal polypeptide-like immunoreactive mucosal endocrine cells and nerve fibres in all layers of the gut wall, were detected by both immunofluorescence and peroxidase-antiperoxidase methods. In the other two species, R. esculenta and B. bombina, no mucosal endocrine cells were detected although the vasoactive intestinal polypeptide-immunoreactive nerve fibres were plentiful. Radioimmunoassay showed the presence of significant amounts of vasoactive intestinal polypeptide-immunoreactivity in intestinal extracts from all species. The highest quantities were present in those anurans with both immunostained cells and nerves. Gel permeation chromatography showed that most of the vasoactive intestinal polypeptide-like peptide eluted in a position identical to that of natural mammalian (porcine) vasoactive intestinal polypeptide. The results indicate that a vasoactive intestinal polypeptide-like peptide is well represented in the Anura and that it is immunologically very similar to the mammalian peptide.

Animals↗
PubMed1987

The relationship between intestinal crypt cell production and intestinal water absorption measured in vitro in the rat.

In studies on intestinal adaptation it is often important to obtain contemporaneous data on the rate of cell production and the functional status of the intestine. The measure of the rate of accumulation of vincristine arrested metaphases in microdissected intestinal crypts to determine the crypt cell production rate (CCPR), is one of the most effective methods of estimating intestinal epithelial cell proliferation which is robust enough to withstand scrutiny. However, studies in the field of intestinal adaptation could be much more informative if a valid measure of intestinal function could also be included. One such method is the water absorption capacity in vitro. The intraperitoneal injection of vincristine sulphate (1 mg/kg) had no significant effect on the water absorption capacity of the small intestine, as measured by the segmented flow single pass perfusion method; thus the CCPR of the jejunum and intestinal water absorption were both measured in 19 groups of hypo- and hyper-proliferative rats which should have been in a relatively 'steady state' of cell production and turnover. The minimum values were obtained after hypophysectomy and the maximum values were observed in lactation. CCPR and absorption were significantly correlated (P less than 0.001) with each other. There was a significant (P less than 0.001) correlation between both CCPR and absorption and dry weight of the intestinal segment studies with food intake. Body weight was a poor predictor of either CCPR or absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

The glycosylation of rat intestinal Muc2 mucin varies between rat strains and the small and large intestine. A study of O-linked oligosaccharides by a mass spectrometric approach.

The large glycosylated domains obtained from the rat intestinal mucin Muc2 were isolated from the large and small intestine of the inbred rat strains GOT-W and GOT-BW. The expression of the rat Muc2 in the large intestine was confirmed immunochemically and by Northern blotting. Released oligosaccharides were structurally characterized by gas chromatography-mass spectrometry (neutral and sialylated species) or by tandem mass spectrometry (sulfated species), and a total of 63 structures was assigned. The large intestinal oligosaccharides were found to be identical between the strains, while the small intestinal glycosylation differed. Until now, detailed structural analysis of oligosaccharides isolated from a single mucin core or mucin domain with different origin have not been performed, and the information of different mucin glycoforms has been limited to immunochemistry. Blood group A-determinants (GalNAcalpha1-3(Fucalpha1-2)Galbeta1-, and structures related to the blood group Sda/Cad-related epitope NeuAc/NeuGcalpha1-3(GalNAcbeta1-4)Galbeta1-, were found in GOT-BW small intestine, and also in both large intestines. Blood group H-determinants and NeuAc/NeuGcalpha1-3Galbeta1- were found in all samples. Core 1 (Galbeta1-3GalNAcalpha1-), core 2 (Galbeta1-3(GlcNAcbeta1-6)GalNAcalpha1-), core 3 (GlcNAcbeta1-3GalNAcalpha1-), and core 4 (GlcNAcbeta1-3(GlcNAcbeta1-6)GalNAcalpha1- were also found in all the samples. The large intestine were enriched in sulfated oligosaccharides and the small intestine contained higher amounts of sialylated species. Sulfation were found exclusively on C-6 of GlcNAc.

ABO Blood-Group System↗
PubMed2006

Transcriptional regulation of the glucose-6-phosphatase gene by cAMP/vasoactive intestinal peptide in the intestine. Role of HNF4alpha, CREM, HNF1alpha, and C/EBPalpha.

Gluconeogenesis is induced in both the liver and intestine by increased cAMP levels. However, hepatic and intestinal glucose production can have opposite effects on glucose homeostasis. Glucose release into the portal vein by the intestine increases glucose uptake and reduces food intake. In contrast, glucose production by the liver contributes to hyperglycemia in type II diabetes. Glucose-6-phosphatase (Glc6Pase) is the key enzyme of gluconeogenesis in both the liver and intestine. Here we specify the cAMP/protein kinase A regulation of the Glc6Pase gene in the intestine compared with the liver. Similarly to the liver, the molecular mechanism of cAMP/protein kinase A regulation involves cAMP-response element-binding protein, HNF4alpha, CAAT/enhancer-binding protein, and HNF1. In contrast to the situation in the liver, we find that different isoforms of CAAT/enhancer-binding protein and HNF1 contribute to the specific regulation of the Glc6Pase gene in the intestine. Moreover, we show that cAMP-response element binding modulator specifically contributes to the regulation of the Glc6Pase gene in the intestine but not in the liver. These results allow us to identify intestine-specific regulators of the Glc6Pase gene and to improve the understanding of the differences in the regulation of gluconeogenesis in the intestine compared with the liver.

Animals↗
PubMed1997

Comparison of effects of uroguanylin, guanylin, and Escherichia coli heat-stable enterotoxin STa in mouse intestine and kidney: evidence that uroguanylin is an intestinal natriuretic hormone.

BACKGROUND: Uroguanylin and guanylin are intestinal peptides that activate a receptor-guanylate cyclase, which is also a receptor for Escherichia coli heat-stable enterotoxin (STa). These peptides may have a role in the body's regulation of fluid and electrolytes. METHODS: STa, bioactive guanylin, and bioactive uroguanylin were evaluated for effects in: 1) the suckling mouse intestinal fluid secretion assay; 2) an in vitro suckling mouse intestinal loop assay; 3) an intestinal receptor autoradiography assay; 4) a control or agonist-stimulated assay for cGMP response in T84 cells; and 5) an in vivo renal function assay in mice. RESULTS: In vivo, orally administered uroguanylin and STa but not guanylin, stimulated intestinal fluid secretion. All three peptides activated intestinal guanylate cyclase and had common intestinal receptors. In vitro, after pretreatment with chymotrypsin, only uroguanylin and STa retained agoinst activity. Chymostatin preserved guanylin activity. STa and uroguanylin induced diuresis, natriuresis, and kaliuresis. Guanylin was less potent than uroguanylin and STa. CONCLUSIONS: The results suggest that the endogenous intestinal peptides, uroguanylin and guanylin, regulate water and electrolyte homeostasis both through local effects on intestinal epithelia and endocrine effects on the kidney.

Animals↗
PubMed1982

Intestinal mucinous substances in gastric intestinal metaplasia and carcinoma studied by immunofluorescence.

Immunofluorescent studies using specific antisera against intestinal mucins revealed small intestinal mucin antigen (SIMA) and large intestinal mucin antigen (LIMA) in areas of intestinal metaplasia of the stomach. In 25 gastric carcinomas studied, both these antigens were detected in seven carcinomas, SIMA only was present in four and LIMA in only four cases; the antigens could not be detected in ten of the carcinomas. In 21 of the 25 gastric operation specimens, including the 15 carcinomas positive for intestinal mucin antigens, there was evidence of chronic gastritis and intestinal metaplasia. These immunohistologic observations confirm the results of recent histochemical studies that both small and large intestinal type mucins are present in intestinal metaplasia and gastric carcinomas. Our findings provide further evidence that at least a proportion of gastric carcinomas may supervene on intestinal metaplasia. The absence of one or both antigens in gastric carcinomas may indicate stages of dedifferentiation or alternatively differences in histogenesis.

Adenocarcinoma, Mucinous↗
PubMed1996

The effect of allopurinol pretreatment on intestinal hypoperfusion encountered after correction of intestinal volvulus.

After reversal of blood flow following a prolonged period of ischemia, blood flow returns for a few seconds and is reduced afterward. This is called "no-reflow phenomenon." Antioxidants such as allopurinol have been shown to prevent the occurrence of this phenomenon in organs other than the intestine. An experimental study was conducted to investigate the effect of allopurinol pretreatment on intestinal blood flow after correction of intestinal volvulus in rabbits. In group 1, baseline intestinal blood flow (IBF) was evaluated using radiolabeled red blood cells. In group 2, 720 degrees intestinal volvulus was created and IBF was evaluated 6 hours later. In group 3, intestinal volvulus was created and devolvulus was performed 6 hours later. Intraperitoneal isotonic saline was injected 60 minutes before correction of the volvulus. IBF was evaluated after correction of the volvulus. Group 4 had the same procedures as group 3, but allopurinol (200 mg/kg) was injected in place of the isotonic saline. IBF stopped 6 hours after volvulus. Compared with the baseline group, IBF was significantly lower in the group with volvulus + devolvulus (P < .01). The IBF of the allopurinol-treated group was significantly higher than that of the isotonic saline group (P < .01) and it did not differ significantly from that of the baseline group. Histopathological examination showed that intestinal volvulus leads to histological injury. The histological injury was more pronounced in the devolvulus group and was less severe in the allopurinol group in comparison to the isotonic saline pretreatment group (P < .01). It is concluded that allopurinol pretreatment prevents the intestinal hypoperfusion (no-reflow phenomenon) and histological injury encountered after correction of intestinal volvulus of 6 hours' duration.

Allopurinol↗
PubMed1998

Involvement of intestinal P-glycoprotein in the restricted absorption of methylprednisolone from rat small intestine.

The interaction between steroid hormones and intestinal P-glycoprotein was investigated by measuring intestinal absorption from rat small intestine in situ. Prednisolone and hydrocortisone were rapidly absorbed from the entire small intestine. In contrast, methylprednisolone absorption was significantly retarded in jejunum and ileum by an intestinal efflux system. In the presence of verapamil an quinidine, the retarded absorption of methylprednisolone was completely recovered, suggesting that P-glycoprotein is responsible for the unique features of methylprednisolone absorption. A requisite for the substrate of intestinal P-glycoprotein seemed to be 6 alpha-methyl group in the steroid structure. Substrate specificity of intestinal P-glycoprotein to steroid hormones was shown to be in part different from those in other tissues such as adrenal gland. Little of all three steroid hormones disappeared in the supernatant of mucosal homogenate from rat small intestine, indicating that intestinal metabolism of these steroid hormones was relatively small.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Spontaneous localized intestinal perforation and intestinal dilatation in very-low-birthweight infants.

AIM: To elucidate how spontaneous localized intestinal perforation (SLIP) is related to intestinal morphological features such as dilatation in very-low-birthweight (VLBW) infants. METHODS: The medical records of 13 VLBW infants (<1500 g) undergoing laparotomy between 1983 and 2003 for presumed SLIP were retrospectively reviewed. Clinical findings including maternal, prenatal and perinatal factors were analysed, and the clinical and surgical findings upon laparotomy were compared. RESULTS: Postnatal pathological conditions included patent ductus arteriosus (n=7), sepsis (n=2), respiratory distress syndrome (n=7), intraventricular haemorrhage (n=2), an indwelling catheter via the umbilical vein (n=1) and pneumonia (n=1). Indomethacin was used in seven neonates with patent ductus arteriosus, and dexamethasone preventive therapy was employed in one neonate for bronchopulmonary dysplasia. Operative findings revealed a localized small punched-out perforation in the ileum. Five patients had intestinal dilatation: two with a perforation in the middle of the dilated intestine, and three with a perforation proximal to the region of dilatation. The muscularis propria was absent in the dilated intestine of four patients. CONCLUSION: This study found no significant relationship between perforation and dilatation of the intestine. Perforation may occur in any portion of the ischaemic intestine when circulatory failure becomes severe, and is not necessarily restricted to the dilated intestine. We believe that SLIP and intestinal dilatation may occur on the same basis in low-birthweight infants; however, the disease process may be aetiologically different.

Dilatation, Pathologic↗
PubMed2002

Pathogenesis of paralytic ileus: intestinal manipulation opens a transient pathway between the intestinal lumen and the leukocytic infiltrate of the jejunal muscularis.

OBJECTIVE: To investigate the existence of a pathway between intraluminal products and the muscularis leukocytic infiltrate. SUMMARY BACKGROUND DATA: Mild intestinal manipulation or lipopolysaccharide initiates an intense inflammatory response within the intestinal muscularis, resulting in paralytic ileus. A major potential morbidity factor in ileus is luminal bacterial overgrowth. METHODS: ACI rats were subjected to small bowel manipulation, after which fluorescent carboxylated or paramagnetic microspheres were administered into the gut lumen. Animals were killed between 0 and 24 hours; unoperated rats served as controls. RESULTS: Intestinal manipulation led to an early transient transference of microspheres from the intestinal lumen into mesenteric lymph that was not observed in unmanipulated controls. A time- dependent, significant increase in microsphere-laden phagocytes was observed within the intestinal muscularis. Immunohistochemistry and electron microscopy of the intestinal muscularis identified the phagocytes as extravasating ED1+ monocytes. Interruption of the lymphatics abolished the accumulation of microsphere-laden monocytes within the muscularis, although a significant monocytic recruitment could still be observed within the intestinal muscularis. CONCLUSIONS: These data show that intestinal manipulation leads to a transient increase in mucosal permeability and that the extraintestinal endocytotic uptake of transferred particles by circulating monocytes precedes their infiltration into the gut wall. The transference of luminal bacterial products may follow a similar route and time course as the microspheres. The authors hypothesize that endogenous bacterial products act synergistically with the inflammatory response within the postsurgical intestinal muscularis, leading to an exacerbation of postoperative ileus.

Animals↗
PubMed1992

Intestinal function following allogeneic small intestinal transplantation in the rat.

This study tests the hypothesis that small bowel transplantation alters the function of the intestine. The function of the small intestine was investigated after syngeneic (BN----BN or Lew----Lew) and fully allogeneic (BN----Lew) orthotopic total small intestinal transplantation (SIT) using a two-stage model. All animals were treated with cyclosporine A throughout the 60-day study period. Syngeneic transplantation reduced weight gain in the (BN----BN) rats, but not in the (Lew----Lew) animals. Allogeneic transplantation caused a reduction in weight gain for the first 30 days posttransplantation, which may have been associated with graft-versus-host disease. Thereafter, the rate of growth of allogeneic SIT animals was normal. Dietary fat absorption was reduced in all groups of transplanted animals. Intestinal permeability to mannitol and polyethylene glycol 400 (PEG-400) was increased by syngeneic transplantation in all groups, with further permeability increases to mannitol, lactulose, PEG-400, and 51Cr-EDTA after allogeneic SIT. The glucose-stimulated intestinal short circuit current was reduced by both syngeneic and allogeneic SIT, but the maximal active transport rate for glucose uptake was increased, as was the passive uptake of fatty acids. These functional alterations were not associated with changes in intestinal morphology or evidence of rejection. These findings demonstrate that: (1) SIT results in significant changes in the transport characteristics of the bowel, but these have a minimal impact on the well-being of the animal overall; (2) SIT induces an increase in intestinal permeability to mannitol and PEG-400, with a further increase in permeability to all markers following allogeneic SIT; (3) following SIT, and the immune events associated with allogeneic SIT, significant adaptation of the transplanted intestine occurs. We suggest that denervation of the small intestine after SIT is the underlying cause of the changes observed.

Animals↗
PubMed2006

Neural mechanisms involved in the inhibition of intestinal motility induced by intestinal electrical stimulation in conscious dogs.

The effects and mechanisms of intestinal electrical stimulation (IES) with long pulses on intestinal motility were investigated in conscious dogs. Eighteen dogs were equipped with serosal electrodes and an intestinal cannula in the small bowel. The first experiment was designed to study the effect of one-channel IES on intestinal motility and the extent of this effect. The second experiment was conducted to study the effect of IES on intestinal motility and the involvement of neural pathway. The IES with long pulses significantly inhibited intestinal motility. Intestinal motility of the entire measured segment (40-220 cm distal to the stimulation electrodes) was inhibited by 60-74% with the single-channel IES with long pulses. Hexamethonium, guanethidine, phentolamine, propranolol partially, but not N(omega)-nitro-L-arginine (L-NNA), ondansetron and naloxone prevented the inhibitory effect of IES on intestinal motility. We conclude that single-channel IES inhibits intestinal motility within a distance of at least 2 m. This inhibitory effect induced by IES with long pulses is mediated via sympathetic but not nitrergic, serotoninergic 5-HT(3) and opiate pathway.

Animals↗