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PubMed2001

Effects of intestinal transplantation on postprandial motility and regulation of intestinal transit.

BACKGROUND: The effects of intestinal transplantation on gut motility have not been completely defined. In this study we examine the effects of ileal transplantation on ileal smooth muscle contractility, together with gastroduodenal emptying, intestinal flow, and transit rates in a canine model of short-gut syndrome. METHODS: Animals (n = 22) were instrumented with strain gauge transducers, collection cannulae, and infusion catheters to assess motility, intestinal flow and transit rates, and gastroduodenal emptying. Ten animals served to define normal parameters. Six animals underwent a 70% resection of the proximal small intestine to serve as short-gut controls. Six animals underwent removal of a 100-cm segment of the ileum, with cold storage, and autotransplantation the following day combined with a 70% resection of proximal bowel. RESULTS: Transplant animals exhibited delayed gastroduodenal emptying, reduced intestinal flow rates, and postprandial phasic contractions that were similar to short-gut controls. However, transplant animals experienced rapid intestinal transit compared with short-gut controls (4.8 +/- 0.4 cm/min vs 2.0 +/- 0.3 cm/min; mean +/- SEM; P <.05). CONCLUSIONS: The transplanted intestine, even with 18 hours of cold storage, exhibits a relatively normal postprandial motor response. However, adaptive responses of the transplanted intestine, such as regulation of intestine transit, may be impaired by neuromuscular injury associated with denervation or ischemia.

Animals↗
PubMed2000

Changes in intestinal villi, cell area and intracellular autophagic vacuoles related to intestinal function in chickens.

1. Morphological changes in the intestinal villi, cell area and cell mitosis number in the duodenal epithelial cells were compared in cockerels fasted for 1, 2 and 3 d, and also when refed for 1 and 2 d after 3 d of fasting, to demonstrate whether these morphological changes are related to intestinal function. Alterations in the fine structure of vacuoles in epithelial cells were also examined in each group to investigate whether the vacuolar changes are associated with these morphological changes, and to obtain an index for judging the nutritional condition of the chicken intestine. 2. Fasting induced decreases in villus height, cell area and cell mitosis number, which recovered rapidly after refeeding, suggesting that these parameters are related to changes in intestinal function and may be useful for assessing intestinal function. 3. At 1 d of fasting, small electron-dense bodies appeared in the absorptive epithelial cells, some of them fusing with each other. As the fasting period increased, these small bodies developed to moderate-sized nascent autophagic vacuoles containing various kinds of electron-dense contents and finally became large autophagic vacuoles with electron-lucent contents. Some vacuoles showed positive acid phosphatase reactions, which indicated that they were lysosomal autophagic vacuoles containing hydrolytic enzymes. 4. After 1 d of refeeding the large autophagic vacuoles seen after 3 d fasting rapidly decreased to the small electron-dense bodies seen after 1 d of fasting. 5. These findings suggest that intestinal epithelial cells have the ability to digest their own cell components to supply nutrients during fasting by means of lysosomal active autophagic transport mechanisms: after refeeding, the epithelial cells return to the absorption of nutrients. 6. The present results demonstrate that the autophagic vacuolar changes are correlated with changes in intestinal villus height, cell area and cell mitosis number induced by fasting and refeeding; this indicates that autophagic vacuoles are a useful index of the nutritional condition of chicken intestine. The greater the number of electron-lucent vacuoles there are in the duodenal absorptive cells, the lower the nutritional condition of the chicken intestine.

Animals↗
PubMed1996

A surgical model to increase the intestinal absorptive surface: intestinal lengthening and growing neomucosa in the same approach.

Despite numerous investigations short bowel syndrome (SBS) is still an unsolved clinical problem. The purpose of this study was to develop a new surgical approach that combines both intestinal lengthening and growing neomucosa. The operative principle is based on a longitudinal division of an intestinal segment antimesenterically and a formation of two intestinal tubes out of bowel halves anastomosing one cutting edge to the incised mucosal midline and the other to the antimesenteric side of the constructed first intestinal tube, so that a common wall between the two hemiloops was created which leads to grow neomucosa. This procedure was applied to 11 rabbits. The hemiloops and neomucosa were investigated for its feasibility and morphologic characteristics. Gross and microscopic examinations at 8 weeks revealed that all the intestinal tubes were viable and patent. No anastomotic leakage was present. In all animals, the serosal surfaces of the common walls were covered with neomucosa that resembles the mucosa of the existing intestine morphologically; there was no significant difference in villus height, villus width at base, crypt depth, number of villi per unit serosal length, villus surface, and villus surface per unit serosa. The growth of neomucosa was completely a result of epithelialization without any evidence of contraction. The quantity and rate of neomucosal growth seems unaffected by intestinal segment length. Finally a two times increase in intestinal length, whereas the diameter halved and a statistically significant increase (P < 0.001) in total villus surface via growing neomucosa was obtained. This model might be useful in the management of SBS when supported by clinical and functional investigations.

Animals↗
PubMed1987

Vasoactive intestinal polypeptide actions on the guinea pig intestinal mucosa during neural stimulation.

Electrical stimulation of the mucosal innervation of the guinea pig ileum results in an increase in chloride secretion that is mediated in part by excitation of muscarinic cholinergic receptors on enterocytes. This study investigated the involvement of vasoactive intestinal peptide in the cholinergic and noncholinergic phases of the secretory response evoked by electrical stimulation of submucosal neurons in the guinea pig ileum. Flat sheets of ileum set up in Ussing flux chambers responded to exogenous vasoactive intestinal peptide by an increase in baseline short-circuit current which was reduced by furosemide and by vasoactive intestinal peptide antiserum. When submucosal neurons were electrically stimulated, a biphasic change in short-circuit current was evoked. Vasoactive intestinal peptide, forskolin, and isobutylmethylxanthine enhanced the cholinergic portion of the response, whereas the antiserum prevented or reduced the effects of the peptide but not of forskolin. In the presence of atropine to eliminate the cholinergically mediated response, vasoactive intestinal peptide reduced the noncholinergic phase of the response and its action was prevented by the antiserum. Vasoactive intestinal peptide enhanced the increase in short-circuit current evoked by the muscarinic agonist bethanechol. These results demonstrate that vasoactive intestinal peptide and other substances that stimulate secretion by increasing cyclic 3',5'-adenosine monophosphate levels in enterocytes potentiate the calcium-dependent, cholinergic phase of the chloride secretory response evoked by neural stimulation of the guinea pig ileum. No evidence was found for vasoactive intestinal peptide as the mediator of the noncholinergic phase of the response.

Animals↗
PubMed1992

Distributions of neuropeptide Y, vasoactive intestinal peptide and somatostatin in populations of postganglionic neurons innervating the rat kidney, spleen and intestine.

Some peripheral peptidergic nerves selectively innervate different types of tissue in abdominal organs. Neuropeptide Y- and vasoactive intestinal peptide-immunoreactive nerve terminals have been identified in the kidney, spleen and intestine and these peptides may have important physiological actions. Somatostatin has been found in sympathetic ganglia, and nerve terminals containing this peptide have been identified in the intestine. We have used fluorescent retrograde tracers to identify renal, splenic and mesenteric postganglionic neurons in rat sympathetic ganglia and then used immunocytochemistry to determine the proportions of these three identified groups of neurons displaying immunoreactivity for neuropeptide Y, vasoactive intestinal peptide and somatostatin. Most renal, splenic and mesenteric neurons were immunoreactive for neuropeptide Y and less than 1% of cells innervating these organs were immunoreactive for vasoactive intestinal peptide. Somatostatin immunoreactivity was present only in a small percentage of mesenteric neurons and not in renal or splenic neurons. The present study demonstrates that (i) the rat kidney, spleen and intestine do not differ in the proportion of innervation by neuropeptide Y-immunoreactive neurons, (ii) the solar plexus, splanchnic ganglion and chain ganglia (T12 and T13) provide very little vasoactive intestinal peptide-immunoreactive inputs to these organs, and (iii) somatostatin-immunoreactive neurons innervate the intestine but not the kidney or spleen.

Animals↗
PubMed2001

Retention and transit of intestinal mucoadhesive films in rat small intestine.

The retention and transit characteristics of intestinal mucoadhesive film systems have been studied after intraduodenal administration in rats. Small size four layered film preparations, 0.5x0.5 mm, were prepared, where the backing layer (45.1+/-2.9 microm thick) was made of a water-insoluble polymer, ethylcellulose (EC), the surface layer was made of enteric pH-sensitive polymers, Eudragit L100, S100 or HP-55 and the middle layer was made of cellulose membrane. The surface layer was attached to the middle layer with an adhesive layer composed of carboxyvinyl polymer (Hiviswako(R) 103). After administration of ten films to the duodenum, the rats were sacrificed hourly and the distribution of the films in the whole small intestine was directly observed after abdominal incision. The HP-55, Eudragit L100 and S100 film systems were found to adhere to the upper, middle and lower part of the small intestine after 1, 2 and 4 h, respectively, for 2-3 h. Direct inspection study suggests that intestinal mucoadhesive film system has functions of: (1) pH-dependent intestinal adhesion site specificity; (2) adhesion to the intestinal wall; and (3) retention in the small intestinal adhesion site for at least 2 h. Intestinal mucoadhesive film system has been suggested to be a targeting system for drugs to the gastrointestinal tract.

Adhesiveness↗
PubMed2003

Adult worms of the rodent intestinal nematode, Strongyloides venezuelensis, successfully invade chick intestinal mucosa.

In order to study the mucosal invasion of a rodent intestinal nematode in bird intestine, chicks were infected with the intestinal nematode of rodents, Strongyloides venezuelensis, by subcutaneous larva inoculation and adult worm implantation. No evidence was obtained for larvae reaching the lungs or the intestine after infective larva inoculation. Adult worms implanted in the small intestine invaded the mucosa and remained there at least for 24 h, whereas those implanted in the caecum were trapped by mucus, and did not invade the mucosa. Mucosal invasion of adult worms in the small intestine was confirmed by histological examination. The number of adult worms in the intestinal mucosal tissue dropped rapidly within the first 24 h, which was associated with infiltrating granulocytes around the worms. The present study suggests that S. venezuelensis adult worms are able to invade the intestinal tissue of chicks, which do not belong to the vertebrate class of its normal definitive host, but that they are eliminated rapidly by mucosal defense system of the bird.

Animals↗
PubMed2001

Down-regulation of intestinal scavenger receptor class B, type I (SR-BI) expression in rodents under conditions of deficient bile delivery to the intestine.

Scavenger receptor class B, type I (SR-BI) is expressed in the intestines of rodents and has been suggested to be involved in the absorption of dietary cholesterol. The aim of this study was to determine whether intestinal SR-BI expression is affected in animal models with altered bile delivery to the intestine and impaired cholesterol absorption. SR-BI protein and mRNA levels were determined in proximal and distal small intestine from control, bile-duct-ligated and bile-diverted rats and from control and bile-duct-ligated mice. Two genetically altered mouse models were studied: multidrug resistance-2 P-glycoprotein-deficient [Mdr2((-/-))] mice that produce phospholipid/cholesterol-free bile, and cholesterol 7alpha-hydroxylase-deficient [Cyp7a((-/-))] mice, which exhibit qualitative and quantitative changes in the bile-salt pool. Cholesterol-absorption efficiency was quantified using a dual-isotope ratio method. SR-BI was present at the apical membrane of enterocytes in control rats and mice and was more abundant in proximal than in distal segments of the intestine. In bile-duct-ligated animals, levels of SR-BI protein were virtually absent and mRNA levels were decreased by approximately 50%. Bile-diverted rats, Mdr2((-/-)) mice and Cyp7a((-/-)) mice showed decreased levels of intestinal SR-BI protein while mRNA levels were unaffected. Cholesterol absorption was reduced by >90% in bile-duct-ligated and bile-diverted animals and in Cyp7a((-/-)) mice, whereas Mdr2((-/-)) mice showed an approximately 50% reduction. This study shows that SR-BI is expressed at the apical membrane of enterocytes of rats and mice, mainly in the upper intestine where cholesterol absorption is greatest, and indicates that bile components play a role in post-transcriptional regulation of SR-BI expression. Factors associated with cholestasis appear to be involved in transcriptional control of intestinal SR-BI expression. The role of SR-BI in the cholesterol-absorption process remains to be defined.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1992

Increases in intestinal glucose absorption and hepatic glucose uptake elicited by luminal but not vascular glutamine in the jointly perfused small intestine and liver of the rat.

1. Previous studies have shown that an arterial-to-portal glucose concentration gradient may be an important signal for insulin-dependent net hepatic glucose uptake. It is not known whether intestinal factors also contribute to the regulation of hepatic glucose utilization. This problem was studied in a newly developed model which allows luminal perfusion of the small intestine via the pyloric sphincter and a combined vascular perfusion of the small intestine via the gastroduodenal artery and superior mesenteric artery, and of the liver via the hepatic artery and portal vein. 2. In both the presence and the absence of 1 mM-glutamine in the vascular perfusate, only about 7% of a luminal bolus of 5500 mumol (1 g) of glucose was absorbed by the small intestine, and nothing was taken up by the liver. 3. With small doses of 75-380 mumol (11-55 mg) of luminal glutamine, but not with 300 mumol of alanine, the intestinal absorption of the luminal glucose bolus was increased almost linearly from 7% to a maximum of 40% and the hepatic uptake from 0% to a maximum of 22%. 4. The increase of hepatic glucose uptake caused by luminal glutamine was only observed when the glucose load was applied into the intestinal lumen, rather than into the superior mesenteric artery. 5. The relative hepatic glucose uptake (uptake/portal supply) was enhanced from 0% to 55% with an increase in portal supply by luminal glutamine, whereas with a similar range of portal glucose supply the relative hepatic uptake by the isolated liver, perfused simultaneously via the hepatic artery and portal vein, was slightly decreased, from 20% to 15%. 6. Addition of various amounts of portal glutamine and/or alterations in the Na+ content of the portal perfusate failed to mimic the luminal glutamine-dependent activation of hepatic glucose uptake. Therefore the luminal-glutamine-elicited activation of hepatic glucose uptake was apparently not caused by a simple increase in the portal-arterial glucose gradient, by glutamine itself or by Na(+)-dependent alterations in hepatic cell volume. The results suggest that luminal glutamine caused not only an increase in intestinal glucose absorption by unknown mechanisms but also the generation of one or more humoral or nervous 'hepatotropic' signals in the small intestine which enhanced the hepatic uptake of absorbed glucose.

Absorption↗
PubMed2003

Small intestinal morphology and activity of intestinal peptidases in piglets around weaning.

The effect of weaning on small intestinal morphology and the activities of three intestinal peptidases was investigated from 3 days prior to weaning to 9 days post-weaning in 64 piglets. Villous height, crypt depth and mitotic counts were determined at three positions along the small intestine. The activities of aminopeptidase N, dipeptidylpeptidase IV and gamma-glutamyl transpeptidase were measured at five positions along the small intestine. The villous height was maximal on the day of weaning. Post-weaning, the villi shortened at the proximal positions of the small intestine and the minimal length was observed on day 3 after weaning. Villous height did not decrease distally in the small intestine. Increased crypt depth was observed from 3-7 days post-weaning at all positions examined. Mitotic counts showed increased proliferative activity in the crypts from the third day post-weaning. Weaning influenced the activity of aminopeptidase N and dipeptidylpeptidase IV. The activities declined until day 3 post-weaning. After that, the activities increased and they had reached pre-weaning values by day 9 post-weaning. Weaning had only minor effect on the activity of gamma-glutamyl transpeptidase. In summary, weaning induced changes in small intestinal morphology and enzyme activity. The changes were maximal on day 3 post-weaning and during the following days, a gradual recovery of the small intestine was observed.

Aging↗
PubMed2006

Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.

OBJECTIVE: Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When exposed to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein interaction, and increased monolayer permeability. Pretreatment with the zonulin antagonist FZI/0 blocked these changes without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from celiac patients in remission expressed a sustained luminal zonulin release and increase in intestinal permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from non-celiac patients demonstrated a limited, transient zonulin release which was paralleled by an increase in intestinal permeability that never reached the level of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS: Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.

Animals↗