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At least 343 records · Page 19Linked to original sources
PubMed1996

Suppression of enterotoxin-induced intestinal fluid secretion by wood creosote.

Wood creosote suppresses intestinal fluid secretion induced by heat-labile enterotoxin (LT) of enterotoxigenic Escherichia coli (ETEC). When rabbit jejunum is ligated into a 5-cm segment and LT is administered locally, it actively induces intestinal fluid secretion in a dose-dependent manner. Local administration of wood creosote together with a fixed dose of LT suppressed the LT-induced fluid secretion in a dose-dependent manner. At a 50-ng/segment dose of LT, 7.4 +/- 1.1 ml (n = 5) of fluid is secreted into an intestinal segment; coadministration of wood creosote (150 micrograms/segment) significantly (p < 0.01) suppressed the fluid secretion to 2.4 +/- 2.3 ml. Based on these results, we conclude that the antidiarrheal activity of wood creosote is attributable to its antisecretory or proabsorptive effect (or both) on the intestine.

Animals↗
PubMed1984

[Chromato-mass-spectral study of the secretion in the rabbit small intestine discharged in response to cholera and salmonella toxins].

A study was made of rabbit small intestine secretion induced by cholera and salmonellosis toxins. Application of electron impact mass-spectrometry and chemical ionization permitted identification of 9 and structure assignment for 14 out of 27 secretion components. The assay demonstrated the major part of the components to be the monosaccharides, glucose and galactose. Fatty acids, cholesterol and hydroxyacids were found to be present in negligible amounts. It was discovered that the action of the toxins primarily affected the metabolism of unsaturated fatty acids.

Animals↗
PubMed1987

Interleukin-1 induces mucus secretion from mouse intestinal explants.

Secretion of goblet cell (GC) mucus occurs during immune reactions in the gut. As human macrophages produce a substance that induces mucus secretion from lung explants, we tested the effect of macrophage-derived factor(s) on mucus secretion from intestinal explants. Fragments of mouse duodenum were incubated with macrophage culture supernatants and purified interleukin-1 (IL-1) preparations, and the amount of mucus released was estimated by an enzyme-linked lectin assay. Both the culture supernatants and the IL-1 preparations induced dose- and time-dependent mucus release. Lipopolysaccharide-induced culture fluids were shown to contain IL-1. Thus, stimulation of mucus secretion from GC can be added to the list of biological activities attributable to IL-1.

Animals↗
PubMed1976

Role of plasma filtration in the intestinal fluid secretion mediated by infection with Salmonella typhimurium.

The mechanisms whereby invasive enteropathogens, e.g., Salmonella typhimurium, induce intestinal secretion are largely unknown. Since these organisms penetrate the intestinal epithelium, disrupt the brush border, and evoke an acute inflammatory reaction, increased plasma filtration through a damaged, more permeable epithelium might contribute to the secretory process. To examine this possibility, the plasma-to-lumen clearance of two different sized molecules, [51Cr]albumin and [14C]mannitol, was measured in the in vivo rabbit ileal loop and in vivo rhesus monkey models of salmonellosis. In the rabbit ileal loop model, the clearance of neither molecule was increased when compared to cholera toxin-exposed loops. In the rhesus monkey, clearance of [14C]mannitol into the jejunum, ileum, and colon of Salmonella-infected animals did not differ from the observed in control animals. These data indicate that invasion of the intestinal mucosa by S. typhimurium has not substantially altered the permeability characteristics of the intestinal mucosa and that plasma filtration through a damaged, more permeable mucosa does not contribute to the Salmonella-induced intestinal secretory process.

Animals↗
PubMed2002

Intestinal bicarbonate secretion by marine teleost fish--why and how?

Intestinal fluids of most marine teleosts are alkaline (pH 8.4-9.0) and contain high levels of HCO(3)(-) equivalents (40-130 mM) which are excreted at a significant rate (>100 microEq kg(-1) h(-1)). Recent research reveals the following about this substantial HCO(3)(-) secretion: (1) It is not involved in acid-base regulation or neutralisation of stomach acid, but increases in parallel with drinking rate at elevated ambient salinities suggesting a role in osmoregulation; (2) In species examined so far, all sections of the intestine can secrete bicarbonate; (3) The secretion is dependent on mucosal Cl(-), sensitive to mucosal DIDS, and immuno-histochemistry indicates involvement of an apical Cl(-)/HCO(3)(-) exchanger. In addition, hydration of CO(2) via carbonic anhydrase in combination with proton extrusion appears to be essential for bicarbonate secretion. The mode of proton extrusion is currently unknown but potential mechanisms are discussed. One consequence of the luminal alkalinity and high bicarbonate concentrations is precipitation of calcium and magnesium as carbonate complexes. This precipitation is hypothesised to reduce the osmolality of intestinal fluids and thus play a potential role in water absorption and osmoregulation. The present studies on European flounder reveal that elevated luminal calcium (but not magnesium) concentrations stimulate intestinal bicarbonate secretion both acutely and chronically, in vitro and in vivo. At the whole animal level, the result of this elevated bicarbonate secretion was increased calcium precipitation with an associated reduction in the osmolality of rectal fluids and plasma. These observations suggest direct functional links between intestinal bicarbonate secretion, divalent cation precipitation and osmoregulation in marine teleost fish.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Effects of calcium channel blockade on intestinal fluid secretion: sites of action.

Most intestinal secretagogues, including cholera toxin, evoke fluid secretion in part by activating the enteric nervous system (ENS). The enterotoxins that, due to size, cannot pass the intestinal epithelial lining have been proposed to activate the ENS via the release of amines/peptides from the intestinal endocrine cells. It has been shown that calcium channel blockers of the L-type attenuate intestinal fluid secretion. This study was performed on rat jejunal segments to elucidate where calcium channel antagonists interact with the secretory nervous reflex(es) of the ENS. In vivo, net fluid transport, transmural potential difference (PD) and luminal release of serotonin from the enterochromaffin cells were monitored before and after exposing the intestinal mucosa to cholera toxin (20 microg/mL) or the calcium ionophore A23187 (0.5 mM). In vitro, the effects of transmural electrical field stimulation (EFS) on short circuit current (SCC) was investigated using the Ussing chamber method. Cholera toxin and A23187 evoked a net fluid secretion, an increased PD and an augmented luminal release of 5-HT. These effects were markedly attenuated by giving the calcium channel blocker nifedipine i.v. (5.75 micromol kg(-1) body wt). On the other hand, nifedipine (0.02 mM) had no significant effect on the increased SCC caused by EFS in vitro. The results obtained in the in vivo experiments suggest that the nifedipine markedly attenuates the initial event in cholera toxin- and A23187-induced secretion, the release of amines and probably also of peptides from the intestinal endocrine cells. The in vitro experiments seem to exclude an effect of the calcium channel blockade on the efferent part of the secretory nervous reflex.

Animals↗
PubMed2002

Thiazolidinone CFTR inhibitor identified by high-throughput screening blocks cholera toxin-induced intestinal fluid secretion.

Secretory diarrhea is the leading cause of infant death in developing countries and a major cause of morbidity in adults. The cystic fibrosis transmembrane conductance regulator (CFTR) protein is required for fluid secretion in the intestine and airways and, when defective, causes the lethal genetic disease cystic fibrosis. We screened 50,000 chemically diverse compounds for inhibition of cAMP/flavone-stimulated Cl(-) transport in epithelial cells expressing CFTR. Six CFTR inhibitors of the 2-thioxo-4-thiazolidinone chemical class were identified. The most potent compound discovered by screening of structural analogs, CFTR(inh)-172, reversibly inhibited CFTR short-circuit current in less than 2 minutes in a voltage-independent manner with K(I) approximately 300 nM. CFTR(inh)-172 was nontoxic at high concentrations in cell culture and mouse models. At concentrations fully inhibiting CFTR, CFTR(inh)-172 did not prevent elevation of cellular cAMP or inhibit non-CFTR Cl(-) channels, multidrug resistance protein-1 (MDR-1), ATP-sensitive K(+) channels, or a series of other transporters. A single intraperitoneal injection of CFTR(inh)-172 (250 micro g/kg) in mice reduced by more than 90% cholera toxin-induced fluid secretion in the small intestine over 6 hours. Thiazolidinone CFTR inhibitors may be useful in developing large-animal models of cystic fibrosis and in reducing intestinal fluid loss in cholera and other secretory diarrheas.

Amino Acid Substitution↗
PubMed2004

Inhibition of rat intestinal Cl- secretion by 4,5-dimethylresorcinol.

Wood creosote, a mixture of phenolic compounds, inhibits enterotoxin-induced intestinal fluid secretion, suggesting that one of its constituents suppresses transepithelial Cl- secretion from the intestinal mucosa. To identify an active constituent in wood creosote that inhibits intestinal Cl- secretion through Cl- channels, we first examined its effect on Cl- secretion using a cultured cell line transfected with complementary DNA encoding a Cl- channel and a Cl- -sensitive fluorescent dye. We next assayed chromatographic fractions of wood creosote for the inhibitory activity on Cl- secretion using a Ussing chamber. We found that 4,5-dimethylresorcinol, identified by gas chromatography-mass spectrometry, inhibited intestinal Cl- secretion dose-dependently when added to a serosal, but not mucosal, surface of rat jejunum, a half-inhibitory concentration being 3.8 microg/ml (28 micromol/l). It was strongly suggested that this effect was due to inhibition of Cl- channels.

Animals↗
PubMed1991

Effect of loperamide on jejunal electrolyte and water transport, prostaglandin E2-induced secretion and intestinal transit time in man.

Jejunal perfusion was performed in 12 healthy volunteers to evaluate the dose dependent effects of loperamide on intestinal absorption, stimulated secretion and transit. In 6 volunteers intestinal perfusion of the jejunal segment with isotonic NaCl solution was followed by addition of loperamide in increasing doses (2-8 mg.l-1). The volunteers were pretreated with 1 mg.l-1 prostaglandin E2 (PgE2) in the perfusate before addition of 4 mg.l-1 loperamide. Phenolsulphonphtalein (PSP) boluses (2 ml) were given to measure mean transit time (MTT). Loperamide 2 mg.l-1 converted the minor secretion after perfusion with the standard solution (water -145 ml.min-1, Na -0.09 and Cl -0.04 mmol.min-1) to absorption (water 0.93 ml.min-1, Na 0.23, Cl 0.25 mmol.min-1) within 15 min. Higher doses of loperamide did not increase absorption. The addition of PgE2 induced net secretion of water (-4.48 ml.min-1) and electrolytes (Na -0.57, Cl -0.51 mmol.min-1). Loperamide 4 mg.l-1 significantly diminished the PgE2-induced net secretion by approximately 50%. Loperamide dose dependently increased the MTT from 6 (2 mg.l-1) to 13.3 min (8 mg.l-1). MTT was still delayed 60 min after a wash out period (10.5 min). It is concluded that loperamide had a dual effect or intestinal activities stimulating absorption and prolonging intestinal transit time with rising doses.

Adolescent↗
PubMed1993

Bicarbonate and citrate in oral rehydration therapy: studies in a model of secretory diarrhea.

In situ perfusion of the rat jejunum and ileum was used to study the effect of inclusion of bicarbonate or citrate on the ability of four oral rehydration solutions to promote small-intestinal absorption of water and sodium. Solutions varied in their sodium (60-90 mM) and glucose (111-140 mM) content and osmolality (281-331 mosmol/kg). They were studied before and after exclusion of base both in normal intestine and in secreting intestine after exposure to cholera toxin. All solutions promoted net water absorption in the normal intestine and reversed net water secretion to absorption in the cholera toxin-treated intestine to varying degrees. Net sodium movement was directly related to the sodium content of oral rehydration solutions. Inclusion of bicarbonate or citrate did not promote significantly greater absorption of water or sodium than did solutions without base, in normal or secreting intestine. In the secreting intestine, inclusion of bicarbonate in two solutions actually resulted in greater sodium secretion than did identical solutions from which bicarbonate was omitted. These studies suggest that the inclusion of base or base precursors in oral rehydration solutions to enhance water and sodium absorption is unjustified in both normal and secreting small intestine.

Animals↗
PubMed1988

The antisecretory factors: inducible proteins which modulate secretion in the small intestine.

1. Cholera toxin and glucose induce the synthesis of antisecretory factors (ASF) of isoelectric points 5.0 and 4.3, respectively, and of a molecular mass of ca 60,000. 2. ASF, in nanogram amounts, inhibit intestinal secretion induced by cholera toxin, Campylobacter toxin, E. coli heat-stable toxin, C. difficile toxin A, and Dinophysis toxin. 3. Intraspinal injection of cholera toxin and glucose induces the synthesis of pituitary ASF much more effectively than does either peroral or intranasal administration. 4. Cholera toxin and glucose seem to act synergistically while inducing ASF. 5. Vagotomy abolishes both the intestinal effects of ASF and the peroral, but not the intraspinal induction of pituitary ASF. 6. ASF has no effect on ion transport across isolated intestinal mucosa from either pig or hen. 7. The results suggest that both the induction and the intestinal effects of ASF are mediated via the central and intestinal nervous system.

Animals↗
PubMed1992

Comparison of the intestinal and serum antibody response in patients with dermatitis herpetiformis.

Dermatitis herpetiformis (DH) is an intensely pruritic, blistering skin disease characterized by cutaneous IgA deposits and an associated, most often asymptomatic, gluten-sensitive enteropathy. When patients with DH are placed on a gluten-free diet both the intestinal abnormality and the cutaneous manifestations of the disease are controlled, suggesting that a mucosal immune response is important in the pathogenesis of DH. Although patients with DH continue to ingest gluten only 40-50% have evidence of an ongoing mucosal immune response in their serum. In order to investigate directly the mucosal immune response in patients with DH the antibody response to dietary antigens was analyzed in intestinal secretions and compared to that found in the serum. Intestinal secretions from six patients with DH and five normal subjects were collected using an intestinal lavage solution and analyzed for total IgA, IgG, IgM, and IgA subclasses, and for IgG, IgA, and IgM antibodies against the dietary antigens bovine beta-lactoglobulin and gliadin. Intestinal secretions from patients with DH contained more IgA than those from normal subjects (mean total IgA: DH = 2.3 mg/ml; normal subjects (NL) = 0.143 mg/ml, P = 0.017). This increase in IgA in intestinal secretions from patients with DH was composed primarily of IgA1 (intestinal IgA: 86% IgA1, 14% IgA2; NL gut secretions: IgA1 = 54%; IgA2 = 46%). Increased IgA antibodies directed against beta-lactoglobulin and gliadin were detected in gut secretions of two of six patients with DH and in none of the normal subjects. Serum IgA antibodies against beta-lactoglobulin and gliadin were detected only in the two subjects who had detectable IgA antibodies in their intestinal secretions. Serum and intestinal IgA anti-beta-lactoglobulin antibodies had similar isoelectric spectrotypes (pI 5.0-6.5), IgA subclass composition, and antigenic reactivity by immunoblot analysis, demonstrating the close relationship between the serum and intestinal IgA antibodies. These data demonstrate that in patients with DH an ongoing mucosal immune response is present in the gut as evidenced by a significantly increased concentration of IgA, predominately IgA1. The strong correlation between detectable serum and intestinal IgA antibodies against dietary antigens demonstrates that the lack of serum IgA antibodies against dietary antigens in some patients with DH is not due to the presence of "blocking" IgA anti-dietary antigen antibodies in intestinal secretions.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Mechanisms underlying the intestinal fluid secretion evoked by nociceptive serosal stimulation of the rat.

Intestinal net fluid transport was measured in vivo continuously with a gravimetric method. Chemical stimulation of the jejunal serosa with hydrochloric acid (0.1 M), ethanol (20%), cat bile or 7-deoxycholic acid (10 mM) evoked an intestinal fluid secretion. Hexamethonium (10 mg/kg b.wt.i.v.) or serosal application of lidocaine (1% solution) partially blocked this secretory response. Bradykinin and prostaglandin E1, two important inflammatory mediators, elicited fluid secretion when applied to the serosal surface at a concentration of 10(-4) M. This secretion was also partly inhibited by hexamethonium. Furthermore indomethacin (10 mg/kg b.wt. i.v.) or pyrilamine (10 mg/kg b.wt. i.v.), a H1-receptor blocker, partly inhibited the secretory response caused by chemical stimulation of the serosa while cimetidine (1 mg/kg b.wt. i.v.), a H2-receptor blocker, had no effect. Freeze sectioned samples from chemically stimulated intestines were examined by fluorescence microscopy. A leakage of i.v. administrated Evans blue labelled albumin into the interstitial space of the serosa and the outer layer of the muscularis was found. It is concluded: The intestinal fluid secretion studied is mainly elicited by nociceptive stimulation of nerves in the serosa or the outer muscularis. The reflex may be activated by the local release of histamine, kinins and prostaglandins. The reflex studied is part of an inflammatory response.

Animals↗
PubMed1982

Relationship between intestinal volume secretion and oxygen uptake.

The effects of net volume secretion on blood flow, oxygen extraction, and oxygen extraction, and oxygen uptake were analyzed in autoperfused segments of cat ileum. Intestinal secretion was induced by local intraarterial infusion of glucagon, histamine, theophylline, prostaglandin E1, or vasoactive intestinal peptide, and, by intraluminal placement of cholera toxin or ricinoleic acid. Net volume secretion rates were determined using a volume recovery method. Intestinal oxygen uptake was increased by all secretagogues. The increases oxygen uptake by the screening intestine resulted from an increased blood flow or oxygen extraction or both. Significant positive correlations between intestinal oxygen uptake and secretion rate were acquired only during cholera toxin, theophylline, and prostaglandin E1, secretion. The results indicate that the metabolic work incurred in the small bowel during secretory states greatly exceeds that reported for the absorptive state.

Alprostadil↗
PubMed1995

Calcium-dependent intestinal chloride secretion by Vibrio parahaemolyticus thermostable direct hemolysin in a rabbit model.

BACKGROUND & AIMS: Vibrio parahaemolyticus is a major agent of seafood gastroenteritis that induces intestinal secretion in the rabbit through its thermostable direct hemolysin. The aim of this study was to characterize the enterotoxicity of purified hemolysin in vitro. METHODS: Rabbit ileum was mounted in Ussing chambers, and changes in potential difference and short-circuit current were monitored after addition of hemolysin. Intracellular calcium concentrations in the nontumoral rat crypt-derived cell line IEC-6 were measured using microspectrofluorometry. RESULTS: In Ussing chamber experiments, mucosal toxin addition up to 50 hemolytic units per milliliter induced a proportional increase of the electrical parameters in normal but not Cl(-)-free Ringer's solution. The response to the toxin was not additive to that of calcium ionophore A23187 and was eliminated by preloading the tissue with 1-2-bis(o-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA), a calcium buffer. In IEC-6 cells, a 10-fold increase in intracellular calcium level was found after addition of hemolysin. Such an increase was totally quenched by BAPTA. Finally, preincubation with trisialoganglioside GT1b, but not monosialoganglioside GM1, eliminated toxin-induced increases in potential difference and short-circuit current. CONCLUSIONS: These data support the hypothesis that the thermostable direct hemolysin induces intestinal chloride secretion using GT1b as a putative receptor and Ca2+ as a second messenger.

Animals↗
PubMed1997

Peptide YY inhibits intestinal Cl- secretion in experimental porcine cryptosporidiosis through a prostaglandin-activated neural pathway.

Peptide YY (PYY) is a powerful inhibitor of intestinal secretion mediated by cAMP agonists such as vasoactive intestinal peptide and prostaglandin E2. We hypothesized that PYY would attenuate the secretory diarrhea in piglet cryptosporidiosis, which is mediated by prostaglandins E2 and I2. Control and infected ileal tissues from piglets were studied in Ussing chambers. The addition of PYY to the serosal bathing solution abolished net Cl- secretion in infected tissue. The inhibitory effect of PYY was eliminated with the prostaglandin synthesis inhibitor indomethacin and with the nerve conduction blocker tetrodotoxin. PYY completely blocked the antiabsorptive and secretory effects of the prostaglandin I2 analog carbacyclin, which has previously been shown to operate through enteric nerve pathways in this tissue. In contrast, PYY had no inhibitory effect on the secretory responses induced by prostaglandin E2 or vasoactive intestinal peptide. Results suggest that the antisecretory effects of PYY are mediated by inhibition of prostaglandin I2 induction of enteric nerves. Thus, PYY may play an important role in moderating the secretory diarrhea in cryptosporidiosis.

Animals↗
PubMed1989

Gamma-interferon-mediated down-regulation of electrolyte secretion by intestinal epithelial cells: a local immune mechanism?

Active chloride (Cl-) secretion by intestinal crypt enterocytes is the central pathophysiological disturbance in most cases of acute diarrhoea. We examined monolayers of the human intestinal cell line T84 mounted in Ussing chambers to see whether the T-cell lymphokine gamma interferon (IFN-gamma) might affect the Cl- secretory properties of these cells, which morphologically and functionally resemble native crypt enterocytes. Pretreatment of T84 cell layers with IFN-gamma for 24 h (but not for 3 h) markedly decreased the Cl- secretory response to vaso-active intestinal polypeptide (VIP) and to cholera toxin and carbachol without appreciably affecting the overall morphology, electrical resistance, or cyclic AMP response of the T84 cell monolayer. The IFN-gamma treatment, however, did induce subtle changes in the T84 cell membrane protein composition which might have affected ion channels regulating Cl- secretion. Our results may indicate a possible novel 'cell-mediated' immune mechanism through which activated gut T cells could modulate the extent of intestinal electrolyte and fluid secretion in, for example, enteric infections.

Carbachol↗