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PubMed1986

Uptake of 450191-S, a 1H-1,2,4-triazolyl benzophenone derivative, in the everted sac of rat small intestine: role of intestinal aminopeptidases.

5-[(2-Aminoacetamido)methyl]-1-[p-chloro-2-(o-chlorobenzoyl)phenyl ]-N,N-dimethyl-1 H-1,2,4-triazole-3-carboxamide hydrochloride dihydrate (450191-S), a sleep inducer, is a ring-opened derivative of 1,4-benzodiazepine and has been reported to be activated by intestinal aminopeptidases in a step of absorption. In this study, we investigated the role of the intestinal aminopeptidases in the uptake of 450191-S by the intestine by using various aminopeptidase inhibitors in everted sacs of rat small intestine in vitro. Glycylglycine did not affect the desglycylation of 450191-S but glycyl-L-leucine or L-leucyl-L-leucine inhibited the reaction. This inhibition was accompanied by reduced concentration of 450191-S metabolites in the intestinal tissue. When the incubation was carried out at 0 degrees C or with puromycin, the desglycylation was also inhibited and the concentration was similarly reduced. Since the extent of inhibition of the desglycylation of 450191-S was negatively correlated with the total concentration of 450191-S metabolites in the intestinal tissue (r = 0.9660), the aminopeptidases must play an important role in the uptake of 450191-S by the intestine. To confirm this, we examined the uptake of the desglycylated product of 450191-S, 8-chloro-6-(2-chlorophenyl)-N,N-dimethyl-4H-1,2,4-triazolo- [1,5-alpha] [1,4]-benzodiazepine-2-carboxamide (M-1) in the same manner. No effect of dipeptides, puromycin or reduced temperature was found on M-1 uptake by the intestine, leading to the conclusion that the aminopeptidases are important for enhancing the uptake of 450191-S in the intestine.

Aminopeptidases↗
PubMed1988

Macroscopic intestinal colonies of mice as a tool for studying differentiation of multipotential intestinal stem cells.

Macroscopic nodules composed of regenerating intestinal epithelium were developed within an area of the murine jejunum ulcerated by X-irradiation (1700 rads). The authors investigated whether such intestinal nodules were clonal and whether this method was useful as a tool for studying differentiation of intestinal stem cells. For examination of the clonality, intestinal nodules were produced in the jejunum of (C57BL/6 X DS)F1-Pgk-1b/Pgk-1a mice that carried X-chromosome inactivation mosaicism for the phosphoglycerate kinase gene. All intestinal nodules contained only 1 type of phosphoglycerate kinase, suggesting the monoclonal origin of nodules. Histochemical and electron microscopic studies showed the presence of absorptive epithelial, goblet, and entero-endocrine cells in most intestinal nodules, suggesting the multipotentiality of the nodule-forming stem cells. Moreover, villi developed on the top of some intestinal nodules, implicating the potential of the multipotential stem cell to construct the highly organized structure. The result indicates that the intestinal nodule method is useful for investigating differentiation potentials of multipotential intestinal stem cells.

Animals↗
PubMed1984

Fetal gastric and small intestine pattern of intestinal mucus antigens in human gastric carcinomas.

The present immunohistological study was performed to investigate the expression of intestinal mucus-associated antigens in the different histological types of gastric carcinoma according to the classification of Laurèn and the WHO classification. We used the following antigenic markers: M3, present in all the goblet cells of the whole small and large intestine; M3SI, expressed in all the goblet cells of the small intestine, but only in some of them of the large intestine; M3D, mainly produced in the upper small intestine; and M3C, specific for colonic mucus cells. All these antigens were found to be similarly expressed in both Laurèn's intestinal and diffuse types. Nevertheless, M3 and M3C appeared to be more largely produced in carcinomas showing well-differentiated cells (tubulopapillary, mucinous, and signet ring cells according to the WHO classification). Our results evidenced the occurrence of two main fetal antigenic patterns in gastric carcinomas, one of the gastric type (M3SI produced to a larger extent than M3 and M3C) and the other one of the small intestinal type (M3 and M3SI more largely expressed than M3C). On the basis of their similar antigenic pattern, the histogenesis of carcinomas showing the fetal small intestinal antigenic profile may be associated with intestinal metaplasia. On the other hand, carcinomas with the fetal gastric pattern may originate from undifferentiated stem cells of the gastric mucosa. Thus, such immunohistological studies could lead to a better understanding of the histogenesis of gastric carcinomas.

Adult↗
PubMed1984

Stable intestinal phenotypic expression of gastric and small intestinal tumor cells induced by N-methyl-N'-nitro-N-nitrosoguanidine or methylnitrosourea in rats.

On the basis of paradoxical concanavalin A (Con A) staining, the tendency of tumor cells of gastric phenotype to shift to intestinal phenotype and the stability of the latter phenotype in stomach tumors of different sizes were examined quantitatively with an image processor. Phenotypic expression of tumors of the small intestine was also studied. One hundred male Wistar rats were given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at 50 micrograms/ml in their drinking water for 20 weeks (group 1). Twenty male F344 rats were given methylnitrosourea (MNU) at a dose of 50 mg/kg ip twice a week for 2 weeks (group 2). Rats in group 1 were killed in week 50 of the experiment and rats in group 2 were killed in week 25. In group 1, the percentage areas of intestinal-type cells in small, medium and large adenocarcinoma of the stomach were 0.5, 2.7 and 6.6%, the differences between these values being significant (P less than 0.05-0.01). Intestinal phenotypic expression of tumor cells of the stomach is stable and the proportion of intestinal-type cells in adenocarcinomas of the stomach is higher in the larger tumors. Adenomatous hyperplasias and adenocarcinomas of the small intestine in groups 1 and 2 were all composed entirely of cells of the intestinal type. These results suggested that intestinal-type cells in adenocarcinoma of the stomach did not originate from intestinal metaplasias but from gastric-type cells in stomach adenocarcinomas.

Adenocarcinoma↗
PubMed1987

The physiology of intestinal oxygenation and the pathophysiology of intestinal ileus.

Intestinal Ileus is Gut Shock caused by Bowel Hypoxia. The morbidity and mortality of Intestinal Ileus has puzzled more than two generations of investigators because they have overlooked the fact that the gas which collects in obstructed small intestine is mostly (90+%) Nitrogen. For some strange reason a gut full of nitrogen has not been looked on as comparable to a lung full of nitrogen, even though the lung and gut have a common embryological origin. My proposal is that intestinal epithelium lining a nitrogen filled lumen becomes as oxygen starved as alveolar lining in a similar circumstance. Bowel hypoxia may be brought about either by failure of the intestine to "breathe out", having breathed in due to mechanical block, or gut paralysis, from any cause, of which one may be failure of blood borne oxygen transport to the bowel, Individually, or together, these may reduce or stop the flow of air and/or aerated intestinal contents along the lumen. Local (bowel) or general underperfusion +/- hypovolaemia +/- anaemia may be a particular cause of paresis or paralysis (aperistalsis) of intestinal muscle. The non-contracting gut then fails to transport the luminal current of fluid and air (oxygen), and adds lumenal to blood-borne oxygen deficiency. The intestinal mucosa utilises oxygen from the current of air churned along the bowel by normal peristalsis to mix with and dissolve in the luminal contents. Should this current be obstructed or the propulsive churning activity cease, oxygen will be "used up", the residual gas become almost entirely nitrogen, and the mucosa must necessarily become oxygen starved and suffocated. Hypoxic mucosa lives in a dangerous environment, at risk of autodigestion by self-produced proteolytic or other enzymes secreted into the lumen by exocrine glands, and it may rapidly become necrotic and gangrenous. Different presentations of Ileus are different degrees of the same Gut Shock due to different levels and durations of tissue hypoxia brought about by different mechanisms with that final common path, complicated by different degrees of autodigestive mucosal destruction, bowel wall oedema, and fluid exudation into the lumen comparable to that through BURNED skin. This idea is new only in so far as it has been put together in this way. Parts have been anticipated by other writers. No new ways of managing ileus are proposed, but it is suggested that existing empirical methods be rationalised and applied more widely and logically.

Acute Disease↗
PubMed2002

Preterm birth affects the intestinal response to parenteral and enteral nutrition in newborn pigs.

Maturation of gastrointestinal (GI) function in neonates is stimulated by enteral nutrition, whereas parenteral nutrition induces GI atrophy and malfunction. We investigated whether preterm birth alters the GI responses to parenteral and enteral nutrition. Pigs were delivered either preterm (107 d gestation) or at term (115 d gestation) and fed total parenteral nutrition (TPN) or enteral sow's milk (ENT) for 6 d after birth. Immaturity of the preterm pigs was documented by reduced blood pH, oxygen saturation and neutrophil granulocyte function, impaired intestinal immunoglobulin G uptake from colostrum, and altered relative weights of visceral organs (small intestine, liver, spleen, pancreas, and adrenals). For both ages at delivery, increases occurred in pancreatic weight (30-75%) and amylase activity (0.5- to 13-fold) after birth, but much more in ENT than in TPN pigs (P < 0.05). Six days of TPN feeding was associated with reduced intestinal weight for both delivery groups (60% of values in ENT, P < 0.001), but only in term TPN pigs was the weight lower than at birth (-20%, P < 0.05). Likewise, it was only in term TPN pigs that intestinal maltase activity increased, compared with ENT, and the absorption of glucose and proline decreased. Only in preterm pigs did TPN feeding increase lactase activity (+50% compared with ENT, P < 0.05). For both delivery ages, the mRNA of lactase-phloridzin hydrolase and sodium-coupled glucose transporter 1 were increased in TPN, compared with ENT. In conclusion, the trophic effect of enteral vs. parenteral nutrition on the GI tract is also present after preterm birth, but the postnatal maturation of many GI functions is modified, compared with term birth. The effects of nutritional regimen on the maturation of the gut epithelium in neonates depend on gestational age at birth.

Animals↗
PubMed1995

Intestinal toxicity of acrylonitrile: in vitro metabolism by intestinal cytochrome P450 2E1.

Acrylonitrile (VCN) is known to cause extensive gastrointestinal damage and tumors in rats. In this study the metabolism of VCN to cyanide (CN-) was characterized in the small intestinal mucosa. The majority of the metabolic reactivity was localized in the microsomal fraction and required reduced nicotinamide adenine dinucleotide phosphate for maximal activity. The intestinal metabolism of VCN to CN- was characterized with respect to VCN concentration, time, pH, and microsomal protein concentration. VCN metabolism to CN- was enhanced significantly by the addition of sulfhydryl compounds such as glutathione, cysteine, and D-penicillamine (10 mM) to 142, 161, and 189% of control, respectively. The intestinal bioactivation of VCN to CN- was enhanced by microsomes obtained from intestinal mucosa of phenobarbital (455% of control), beta-naphthoflavone (375% of control), 4-methylpyrazole (305% of control), or ethanol (165% of control)-treated rats. Addition of ethanol (80 mM) to incubation mixtures containing control or ethanol-induced microsomes resulted in significant inhibition of microsomal metabolism of VCN to CN- to 20 and 34% of control, respectively. Addition of dimethyl sulfoxide induced a similar inhibitory effect on VCN metabolism by control or ethanol-induced microsomes (8 and 26% of control, respectively). Furthermore, antibody to cytochrome P450 2E1, but not antibody to cyt P450 2B1, significantly inhibited VCN metabolism by ethanol-induced intestinal microsomes to about 25% of control. Mild inhibition (80-85% of control) of VCN metabolism was detected when antibody to cyt P450 2B1 or 2E1 was added to incubation mixtures containing Pb-induced intestinal microsomes. These findings indicate that extrahepatic tissues such as the intestinal mucosa are capable of metabolizing VCN to CN- and establish a major role of intestinal cyt P450, particularly cyt P450 2E1, in the intestinal metabolism of VCN to CN-.

Acrylonitrile↗
PubMed1993

Vasoactive intestinal peptide release and L-citrulline production from isolated ganglia of the myenteric plexus: evidence for regulation of vasoactive intestinal peptide release by nitric oxide.

Vasoactive intestinal peptide release and L-[3H]citrulline production were examined in ganglia isolated from the myenteric plexus of guinea-pig intestine. The nicotinic agonist, 1,1-dimethyl-4-phenylpiperizinium stimulated vasoactive intestinal peptide release and L-[3H]citrulline production; the latter was considered an index of nitric oxide production. Both vasoactive intestinal peptide release and L-[3H]citrulline production were abolished by tetrodotoxin, hexamethonium, and the nitric oxide synthase inhibitor, NG-nitro-L-arginine. Inhibition of vasoactive intestinal peptide release by NG-nitro-L-arginine was reversed by L-arginine but not by D-arginine. Exogenous nitric oxide stimulated vasoactive intestinal peptide release whereas exogenous vasoactive intestinal peptide had no effect on L-[3H]citrulline production. The pattern of stimulation by nitric oxide and inhibition by NG-nitro-L-arginine implied that vasoactive intestinal peptide release is facilitated by and may be dependent on nitric oxide production. Consistent with this notion, vasoactive intestinal peptide release in response to either 1,1-dimethyl-4-phenylpiperizinium or nitric oxide was abolished by KT 5823, an inhibitor of cyclic GMP-dependent protein kinase activity and by LY83583, an inhibitor of soluble guanylate cyclase activity. The study provides the first direct evidence of nitric oxide production from enteric ganglia.

Alkaloids↗
PubMed1996

Intestinal motility during ontogeny and intestinal pseudo-obstruction in children.

From the fragmentary studies performed to date of both functional obstruction and the ontogeny of intestinal motility, several conclusions can be drawn. The development of motor activity that is primarily dependent on neuronal activity, such as sucking, swallow-induced peristalsis of the esophagus, and cyclic fasting small intestinal motor activity, occurs according to a timetable that is similar in all species studies is gestationally dependent, but its timing during gestation is species specific. Postprandial events, including gastric emptying and continuous postprandial motor activity in the small intestine, in contrast seem to be dependent on the nature of the humoral response to food, provided that the musculature of the gut and enteric nerves are able to respond to it. Although these activities are primarily determined by neuronal development, there is a limited amount of information to suggest that their appearance may be pharmacologically manipulated to advance the timing and rate of development. It is commonplace now for cortisol to be used to induce the production of surfactant in mothers of babies who are at risk of hyaline membrane disease. A limited amount of information suggests that cortisol may have similar effects in inducing duodenal motor activity, and, thus, it may be possible to advance the timing and rate of development of intestinal motility in the very preterm infant by its use. There are, however, no studies to date to prove this. It is now clear that intestinal pseudo-obstruction is a heterogeneous disorder associated with various pathologies, some of which are intrinsic to the gut, whereas others are multisystem diseases affecting the intestine. In addition, although intestinal pseudo-obstruction was originally thought to involve the small intestine, it is now realized that it may not affect only one region, as in achalasia or Hirschsprung's disease, but also it may present diffusely throughout the gut. The motility changes caused by the disease processes are nonspecific, although neuropathic and myopathic changes are distinct and due to the destruction of the particular motor control system involved. The mechanisms of the ontogenic and disease changes described in this article are, however, almost totally unexplored. The recent upsurge of interest in the area with the development of advances in cellular and molecular biology, at least the early events, is now beginning to unravel. At the present time, the stage is being set for probably the most exciting phase of understanding of the nature of the ontogeny of intestinal motor activity, which the author expects will enable us to manipulate motor activity in normal preterm infants and, it is hoped, congenital dysmotile states.

Animals↗
PubMed1999

Quantitative analysis reveals differential expression of mucin (MUC2) and intestinal trefoil factor mRNAs along the longitudinal axis of rat intestine.

MUC2 and intestinal trefoil factor (ITF) are considered to have important roles in intestinal mucosal protection and epithelial repair. In order to investigate whether these genes are co-ordinately expressed, we have used competitive reverse transcription-polymerase chain reaction assays to measure MUC2 and ITF mRNA levels in human intestinal cell lines and along the longitudinal axis of rat intestine. ITF mRNA was expressed in several intestinal cell lines. However, MUC2 mRNA was detected only in LS174T cells where it was present at approx. 25-fold lower levels than the ITF transcript. In contrast, in rat intestinal tissues, MUC2 mRNA levels were generally higher than ITF mRNA levels. The levels of both transcripts increased markedly during postnatal development. In adult rats, the expression patterns of MUC2 and ITF mRNAs along the longitudinal axis of the small intestine were similar, with lowest levels in the proximal duodenum and relatively constant levels in the other regions assayed. In contrast, the expression patterns of MUC2 and ITF in different regions of the large intestine showed a marked divergence. Our results strongly suggest that expression of the MUC2 and ITF genes is not coordinately regulated in intestinal cells.

Animals↗
PubMed2001

Dietary betaine accumulates in the liver and intestinal tissue and stabilizes the intestinal epithelial structure in healthy and coccidia-infected broiler chicks.

The aim of this experiment was to study the patterns of betaine accumulation into intestinal tissue, liver and plasma of broiler chicks with or without coccidial infection. The chicks were raised on a corn-based, low-betaine diet with or without 1000 ppm betaine supplementation and with or without intestinal microparasite (Eimeria maxima) challenge to the age of 21 days. Plasma, liver, intestinal tissue and digesta of non-challenged (NC) birds and plasma and intestinal tissue of coccidiosis challenged (CC) birds were analysed for betaine content. NC birds were also analyzed for homocysteine in plasma and S-adenosylmethionine (S-AM) in liver. The jejunal epithelium was histologically examined for the presence of coccidia and the crypt-villus ratio was measured. Dietary betaine supplementation decreased the plasma homocysteine concentration but had no effect on liver S-AM of NC birds. The data suggest that chicks on a low-betaine diet accumulate betaine into the intestinal tissue. When the diet was supplemented with betaine, betaine accumulated heavily into liver and to a lesser degree into intestinal tissue. The concentration of betaine in jejunal and ileal digesta was low suggesting that dietary betaine was mainly absorbed from the proximal small intestine. The coccidial challenge decreased the concentration of betaine in the liver, but greatly increased that in the intestinal tissue. The crypt-villus ratio was decreased by the dietary betaine supplementation in healthy and challenged chicks, suggesting that dietary betaine both protects the jejunal villi against coccidial infection and also stabilizes the mucosal structure in healthy broiler chicks. These results support our earlier findings suggesting that betaine is likely to act as an important intestinal osmolyte in broiler chicks.

Animals↗
PubMed1993

The antibody response in serum, intestinal wall and intestinal lumen of NMRI mice infected with Echinostoma caproni.

Groups of mice (NMRI) were infected with 0, 6 and 25 metacercariae of the intestinal trematode Echinostoma caproni. An enzyme linked immunosorbent assay (ELISA) was developed for measuring the specific IgM, IgG and IgA antibody responses in serum, small intestinal tissue and small intestinal lumen of the mice, by using a crude adult E. caproni antigen. In infected mice, significant levels of IgM were measured in the sera from day 14 after infection and of IgG and IgA from day 28 after infection. Early in the infection, the mean level of serum IgM was higher in 6-worm infections than in 25-worm infections. Late in the infection, higher mean levels of IgA were reached in the serum of mice with high than in those with low dose infections. The onset of appearance of antibodies in the tissue of the small intestine reflected the picture seen in the serum. For IgM, and to a lesser degree for IgG, the highest mean antibody levels appeared in the posterior sections of the small intestinal wall, where also the parasites were located. The mean level of IgA, however, was uniform throughout the length of the small intestinal tissue. High levels of specific IgA were detected in the lumen of the small intestine on day 28 after infection, especially in the anterior sections, where only few parasites were located. No specific IgM or IgG could be detected in the intestinal lumen on this day. The results are related to the intestinal location and the pattern of expulsion of E. caproni in the mouse host.

Animals↗
PubMed2001

Proglucagon-derived peptides in intestinal epithelial proliferation: glucagon-like peptide-2 is a major mediator of intestinal epithelial proliferation in rats.

Proglucagon-derived peptides have been implicated in the control of intestinal mucosal cell division. To investigate the actions of these peptides on intestinal cell proliferation, different doses of enteroglucagon, oxyntomodulin, glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) were tested in male Wistar rats maintained on total parenteral nutrition. Crypt cell proliferation was assessed by the analysis of arrested metaphases in microdissected crypts. Enteroglucagon and oxyntomodulin had no effect on intestinal weight or cell proliferation. GLP-1 had a slight effect on stomach and small intestinal weights and on epithelial cell proliferation in the small and large intestines. GLP-2 infusion dose-dependently increased the weights of the stomach, small intestine, colon, and cecum and increased crypt cell proliferation in the small and large intestines of parenterally fed rats. In orally fed animals, GLP-2 increased intestinal weight but had little effect on proliferation. Therefore, of the proglucagon-derived peptides, GLP-2 appears to be a major mediator of intestinal epithelial proliferation.

Animals↗
PubMed2004

Expression of the intestinal marker Cdx2 in the columnar-lined esophagus with and without intestinal (Barrett's) metaplasia.

Barrett's esophagus is diagnosed when goblet cells are found in the lower esophageal mucosa. However, the distribution of these cells is patchy and they may not represent the earliest marker of intestinal metaplasia. Cdx2 is a transcription factor whose expression in normal tissues is restricted to intestinal-type epithelium. Its distribution in the columnar-lined esophagus with and without intestinal metaplasia has been seldom studied. We evaluated Cdx2 expression in lower esophageal biopsies from 90 patients with endoscopic diagnosis of short segment Barrett's esophagus, including 45 consecutive cases showing intestinal metaplasia (goblet cells present in hematoxylin eosin and/or Alcian blue stains) and 45 consecutive cases without goblet cells. 25 samples of cardiac-type mucosa without intestinal metaplasia biopsied from the stomach served as controls. All cases with intestinal metaplasia revealed Cdx2 reactivity in goblet cells and adjacent nongoblet columnar cells. Dysplastic foci, seen in five cases from this group, were Cdx2 positive. In the group without goblet cells, Cdx2 was focally expressed by columnar cells in 17 (38%) cases. All control cases were Cdx2 negative. Strips of Alcian blue-positive nongoblet columnar cells ('columnar blues') were observed in 11 (24%) of the cases without intestinal metaplasia. All these foci were Cdx2 negative. In conclusion, Cdx2 is a highly sensitive marker for Barrett's esophagus. It is also expressed in a significant minority of cases of columnar-lined esophagus without goblet cells, suggesting that it may detect intestinal phenotypic modifications in the absence of goblet cells. Accordingly, Cdx2 immunostaining could help identify patients with Barrett's metaplasia in cases where no goblet cells are visible in biopsies from the columnar-lined esophagus. Finally, lack of Cdx2 expression in the 'columnar blues' suggests that these cells are not diagnostic of intestinal metaplasia.

Adult↗
PubMed2002

Intestinal ischemic preconditioning protects the intestine and reduces bacterial translocation.

Ischemic preconditioning (IPC) was first demonstrated in the heart, but this protective effect has been also recently described in the intestine. The aim of this study was to determine the effects of intestinal ischemic preconditioning on the morphology of intestine and bacterial translocation. Twenty-four male Wistar rats weighting 250 to 300 g were randomized into three groups. A control group of rats (n = 8) were subjected laparotomy. In an ischemic group (n = 8), laparotomy was performed and the superior mesenteric artery was occluded by an atraumatic clamp for 30 min. In the preconditioned group (n = 8), before the ischemia-reperfusion (I/R) period (as in ischemic group), rats were subjected to an initial 10 min of intestinal ischemia and 10 min of reperfusion. Twenty-four hours later, to evaluate whether the I/R induced intestinal injury and bacterial translocation (BT), tissue and blood samples were collected, and liver, spleen, and mesenteric lymph node specimens were obtained under sterile conditions for microbiological analysis. Samples of ileum were removed for both biochemical and histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, liver, and blood was significantly higher than other groups (P < 0.05). IPC prevented I/R-induced BT and it significantly reduced the I/R-induced intestinal injury (P < 0.05). Increased inducible nitric oxide (NO) synthase (iNOS) expression observed on the ileal specimens of the I/R group was found to be prevented by IPC. Our data suggest IPC as a key factor that reduces BT and iNOS activation in intestinal I/R. This is the first study showing that intestinal IPC blocks the cascade of events that causes BT and intestinal injury that may lead to sepsis.

Animals↗
PubMed1986

The influence of intestinal infusion of fats on small intestinal motility and digesta transit in pigs.

The influence of duodenal and ileal infusion of nutrients on small intestinal transit of digesta, measured by the passage of phenol red marker, was studied in twelve pigs fitted with duodenal and ileal catheters, and a terminal ileal cannula. Changes in gastrointestinal motility were observed by electromyography and by use of an X-ray image intensifier in four of the pigs fitted additionally with nichrome wire electrodes in the gut wall and in seven pigs fitted only with a gastric catheter. Small intestinal transit time was unaffected by intestinal catheterization per se, or by duodenal or ileal infusion of glucose or peptone. It was reduced by duodenal infusion of fat or of some of the products of fat digestion including oleic acid and a monoglyceride containing unsaturated fatty acids (monoglyceride LS) but was not affected by infusion of glycerol, stearic acid or a monoglyceride containing saturated fatty acids (monoglyceride P). Ileal transit time was greatly reduced by ileal infusion of soya bean oil mixed with bile salts and lipase and by monoglyceride LS but not by soya bean oil alone. Total small intestinal transit time was reduced to a lesser degree by ileal infusion of soya bean oil mixed with bile salts and lipase and by monoglyceride LS and was unaffected by soya bean oil alone. The level of irregular spiking activity of the small intestine was greatly reduced by both duodenal and ileal infusion of fat, but rapidly propagated spike bursts were initiated from the point of infusion (identified radiologically as peristaltic rushes) many of which travelled right through to the ileo-caecal junction. It is concluded that intestinal infusion of fat accelerates small intestinal transit in pigs by induction of peristaltic rushes; that since the ileal transit times were more severely reduced than total small intestinal transit times by ileal infusion of fat the response is probably only seen over those areas of intestine in direct contract with the fat; and that the effect depends upon the presence of fat digestion products, i.e. the fatty acid and the monoglyceride, although probably only those containing unsaturated fatty acids.

Animals↗
PubMed1992

Non-O1 Vibrio cholerae intestinal pathology and invasion in the removable intestinal tie adult rabbit diarrhea model.

A modified removable intestinal tie adult rabbit diarrhea (RITARD) model was used to investigate the intestinal pathology, intestinal bacterial colonization, intestinal fluid volume, and onset of diarrhea caused by non-O1 Vibrio cholerae. Three strains of non-O1 V. cholerae were studied. RITARD rabbits challenged with 10(3) CFU of strain NRT36S (a strain previously shown to cause diarrhea in volunteers) developed grade 3 diarrhea at 48 to 72 h. The mean counts of non-O1 V. cholerae isolated were 9.3 +/- 0.07 and 8.7 +/- 0.7 CFU/g from the small and large intestines, respectively. Histologic examination showed necrosis of the luminal epithelium in the colon and mild inflammatory cell infiltration in the adjacent lamina propria. The severity and extent of intestinal damage by strain NRT36S was dose dependent. Higher doses of strain NRT36S caused severe necrotizing colitis and enteritis, with bacteremia and mortality at less than 24 h in RITARD rabbits challenged with 10(9) CFU and at less than 48 h in RITARD rabbits challenged with 10(4) CFU. Electron and light microscopy demonstrated invasion of NRT36S into the luminal epithelial cells of the intestine. Challenge of RITARD rabbits with non-O1 V. cholerae A-5 and 2076-79 (strains which did not cause diarrhea in volunteers) did not cause diarrhea or intestinal pathology. Intestinal colonization was transient: at 72 h postchallenge, animals inoculated with strain A-5 were culture negative, while only low numbers of strain 2076-79 were detectable (approximately 0.4 to 0.8 CFU/g). Our data highlight the utility of the RITARD model, when combined with appropriate pathologic and bacteriologic studies, for obtaining insights into pathophysiologic mechanisms of enteric disease by non-O1 V. cholerae. In agreement with volunteer studies, non-O1 V. cholerae NRT36S is clearly pathogenic in this model; direct cell invasion may play a role in its ability to cause illness.

Animals↗
PubMed1991

Regulation of intestinal proglucagon-derived peptide secretion by intestinal regulatory peptides.

The physiological regulation of intestinal proglucagon-derived peptide secretion has not been well studied. We have therefore used a fetal rat intestinal cell culture model to investigate the control of secretion of the gut glucagon-like immunoreactive (GLI) peptides by other intestinal regulatory peptides in vitro. Secretion of the intestinal GLI peptides was found to be stimulated in a dose-dependent fashion by the intestinal endocrine peptide, gastric inhibitory peptide (at greater than or equal to 10(-10) M, P less than 0.05), and by the neurocrine peptides, gastrin-releasing peptide (at greater than or equal to 10(-12) M, P less than 0.05), and calcitonin gene-related peptide (at greater than or equal to 10(-8) M, P less than 0.05). Gastrin-releasing peptide and its amphibian equivalent, bombesin were equipotent in stimulating GLI peptide secretion. In contrast, the endocrine and neurocrine intestinal somatostatin-related peptides, somatostatin-28 and -14, inhibited release of the GLI peptides, at concentrations of 10(-10) (P less than 0.01) and 10(-8) (P less than 0.01) M, respectively, with significant differences in potency between the two peptides detected at 10(-10) M (P less than 0.05). The inhibitory effects of both somatostatin-28 and -14 could be blocked by preincubation of the cells with pertussis toxin (P less than 0.05). Dose-dependent stimulation of gut GLI peptide secretion was also detected in response to treatment of cultured cells with sodium oleate (at 10(-4) M; P less than 0.05), or with the cholinergic agonist bethanecol (at greater than or equal to 100 microM; P less than 0.05). Other endocrine [cholecystokinin, glucagon, glucagon-like peptide-1(1-37), glucagon-like peptide-1(7-37), glucagon-like peptide-2, neurotensin, and peptide YY] and neurocrine (vasoactive intestinal peptide) peptides, and the synthetic glucocorticoid, dexamethasone, were without effect on secretion of the gut GLI peptides, at doses of 10(-12) to 10(-6) M. The results of the present study therefore demonstrate that secretion of the intestinal proglucagon-derived peptides is under the regulatory control of a wide variety of intestinal endocrine and neurocrine peptides, as well as nutrients (fats) and neurotransmitters (acetylcholine).

Animal Nutritional Physiological Phenomena↗