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At least 55 records · Page 3Linked to original sources
PubMed1976

Ion transport changes during calcitonin-induced intestinal secretion in man.

Previous studies have shown that synthetic salmon calcitonin (SCT) infused intravenously causes secretion of water and electrolytes in the jejunum of normal human subjects. The present experiments were carried out to learn more about the nature of this intestinal secretory process. During SCT- or synthetic human calcitonin (HCT)-induced intestinal secretion, the following observations were made: (1) There was no change in potential difference; (2) Cl was secreted against an electrochemical gradient; (3) unidirectional Na flux out of the lumen was decreased while the opposite flux was normal; (4) luminal pCO2 fell; (5) addition of glucose to the jejunal contents stimulated Na abdsorption, and this in turn counteracted the secretory effect of calcitonin. These findings suggest that calcitonin induces active Cl secretion and inhibits active Na absorption, and that HCO3 absorption is reduced by virtue of OH secretion; furthermore, jejunal glucose absorption and glucose-stimulated Na absorption are intact during calcitonin-induced secretion. Intravenous infusion of HCT caused intestinal secretion only when blood levels were much higher than occur physiologically; therefore, calcitonin is probably not a mediator of spontaneous variations of intestinal transport in normal people. However, because calcitonin induces secretion in the ileum as well as in the jejunum, hypercalcitonemia (within the range commonly found in patients with medullary carcinoma of the thyroid) could be a cause of severe secretory diarrhea.

Action Potentials↗
PubMed1984

Intestinal secretion as a cause of hypokalemia and cardiac arrest in a patient with strongyloidiasis.

A 32-year-old white American male contracted strongyloidiasis in Nigeria. Prolonged and severe watery diarrhea was complicated by hypokalemia and cardiac arrest. Steady-state perfusion studies with a plasma-like electrolyte solution revealed net secretion of water, sodium, potassium, and chloride in a segment of jejunum. Mucosal permeability measured by the ratio of [14C]urea and tritiated water diffusion was unchanged. Chloride secretion occurred against both an electrical and chemical gradient, which suggests that chloride secretion was active. Intestinal water and electrolyte secretion may be the mechanism of watery diarrhea in patients with strongyloidiasis.

Adult↗
PubMed1992

Diquat-induced intestinal secretion in the anaesthetized rat.

1. Diquat (1,1'-ethylene-2,2'-bipyridilium) is a non-selective desiccant herbicide which, when administered orally to mammalian species, causes significant secretion of fluid into the lumen of the gastrointestinal tract. In order to characterize this secretory response in more detail the effect of sublethal doses of diquat dibromide (DQBr2) on intestinal secretion was investigated in vivo in the jejunum of anaesthetized rats. 2. Ligated segments of jejunum (10 cm) which were prepared in groups of up to five animals were filled with 500 microliters of isosmotic DQBr2 solutions with concentrations ranging from 1-100 mM and maintained in the anaesthetized rat for 1, 2 or 3 h; in control experiments a solution of 100 mM NaBr was used. 3. It was found that while all of the fluid instilled into the segments was absorbed in the control experiments, there was both a dose- and time-dependent secretory response to DQBr2. Maximal fluid secretion occurred after treatment with 50 mM DQBr2 for 3 h. 4. Histological assessment of the jejunum revealed an increase in cell exfoliation and evidence of luminal distension after incubation with DQBr2. However, no structural damage to the mucosa could be seen to account for the fluid secretion. 5. The model described provides a quantitative means of evaluating intestinal secretion and may be used for elucidating the mechanism by which diquat alters fluid transport processes.

Animals↗
PubMed1975

Methylxanthine induced small intestinal secretion.

Methylxanthines, being potent phosphodiesterase inhibitors, produce increased intestinal cyclic AMP levels and would be predicted to produce increased net intestinal fluid secretion. Their effect when presented to the intestinal lumen, which would be analogous to human ingestion, had not been previously determined. Isolated loops of rat jejunum were perfused with solutions of caffeine and theophylline in vivo. There was a decrease in net fluid absorption in both neonatal and mature animals exposed to theophylline. Mature animals exposed to caffeine developed a prompt secretory response, comparable to thax induced by cholera toxin. The data indicate that methylxanthines are potent intestinal secretagogues when administered intraluminally and suggest that secretory stimulation could be important in the gastrointestinal symptomatology elicited in man by these compounds.

Animals↗
PubMed1985

Incomplete sulphomucin-secreting intestinal metaplasia for gastric cancer. Preliminary data from a prospective study from three centres.

A joint prospective long term study of gastric biopsies has been undertaken to survey intestinal metaplasia Types I, II, and III in terms of their incidence, distribution and value in the selection of high risk cancer patients. This study is based on protocols agreed between three centres for endoscopy, histological interpretation, and mucin histochemistry. The results on the first 1350 gastric biopsies examined during 1981-1982 are presented. Intestinal metaplasia was found in 267 biopsies (20%), being common in association with carcinoma (71%), less so in benign conditions such as gastric ulcer (39%), and chronic gastritis (24%), but rare in 'normal' (3%). Type I intestinal metaplasia was predominant (73%) in all the biopsies with intestinal metaplasia and was most common in benign conditions, 70% in gastric ulcer and 76% in chronic gastritis. Type III intestinal metaplasia (incomplete sulphomucin-secreting intestinal metaplasia) was recorded in only 9.8% of all the biopsies with intestinal metaplasia and had a higher incidence in carcinoma (35%), than in benign conditions (7%) (p less than 0.0001). These results suggest that intestinal metaplasia types may have different malignant potential and their identification may be useful in screening patients for early detection of cancer.

Adult↗
PubMed1998

Inhibition of prostaglandin-induced intestinal secretion by igmesine in healthy volunteers.

BACKGROUND & AIMS: Igmesine, a final sigma ligand, has been shown to inhibit intestinal secretion and diarrhea in animal models. The purpose of this study was to measure the inhibitory effect of igmesine on basal and prostaglandin E2 (PGE2)-induced jejunal secretion in normal volunteers. METHODS: Jejunal absorption of water and electrolytes was measured with a three-lumen open-segment perfusion method in 16 volunteers. A double-blind crossover study was performed involving intraluminal infusion of PGE2 after oral administration of placebo or igmesine at two doses. RESULTS: PGE2 induced net secretion of water and electrolytes (P < 0.01 vs. basal conditions). The effect of PGE2 on water and electrolytes was not changed by 25 mg of igmesine but was suppressed by 200 mg of igmesine. This effect lasted at least 3 hours after a single oral dose. Igmesine at a dose of 200 mg also produced a significant decrease in basal rates of water and electrolyte absorption. CONCLUSIONS: Igmesine, a final sigma ligand, inhibits PGE2-induced intestinal secretion in normal humans. Evaluating the drug in chronic diarrheas may be of interest.

Adult↗
PubMed1981

Effect of chlorpromazine on intestinal secretion mediated by Escherichia coli heat-stable enterotoxin and 8-Br-cyclic GMP in infant mice.

Subcutaneously administered chlorpromazine reduced intestinal fluid accumulation induced by Escherichia coli heat-stable enterotoxin in infant mice. The antisecretory effect of chlorpromazine, although dose related, was, even with high doses, less than that observed with respect to cholera toxin. Whereas 100 micrograms chlorpromazine abolished cholera toxin-induced intestinal secretion almost completely, 500 microgram chlorpromazine (equivalent to 200 microgram/g body wt) lowered secretion induced by heat-stable enterotoxin by only 41%. The effect of chlorpromazine on intestinal secretion was quantitatively similar regardless of whether heat-stable enterotoxin or the cyclic GMP analogue, 8-Br-cyclic GMP, was the secretagogue. This finding, which suggested that the inhibitory effect of chlorpromazine on heat-stable enterotoxin was independent of guanylate cyclase, was confirmed by assaying this enzyme in intestinal homogenates from mice that had been inoculated with chlorpromazine, and also in experiments in which chlorpromazine was added to guanylate cyclase assay mixtures in vitro. Caution is advised before chlorpromazine is routinely adopted for the treatment of all syndromes of watery diarrhea.

Animals↗
PubMed1975

[Hemagglutinating antibodies in the serum and intestinal secretions of rats infested by Nippostrongylus brasiliensis].

Nippostrongylus brasiliensis infected rats responded with the formation of hemagglutinating antibodies in both serum and intestinal secretions. After the first infection seric antibody titers were quite weak but increased sharply after challenge. Intestinal secretion hemagglutinines remained at constant level after both infections. This result represents a new approach in our understanding of the immune mechanism towards this parasite in rats.

Agglutinins↗
PubMed1990

Influence on intestinal secretion of eicosanoids.

Eicosanoids have been shown to be important modulators of intestinal secretion. In cholera, cAMP is often regarded as the sole mediator, but recent data suggest that 5-hydroxytryptamine (5-HT) and prostaglandin (PG) E2 also play important roles. Thus cholera toxin (CT) increases their release from the rat jejunum in vivo, and human cholera is associated with an increased luminal 'overflow' of PGE2. In vitro evidence of secretion can be obtained with PG concentrations 100- to 1000-fold lower than those required for activation of the adenylate cyclase. Furthermore, 5-HT induces secretion associated with increased 'overflow' of PGE2, but without a change in mucosal cAMP. CT-induced release of PGE2 and fluid secretion can be decreased by indomethacin or by the 5-HT2-receptor antagonist, ketanserin, whereas the release of 5-HT and cAMP is not affected by either substance. Secretion caused by vasoactive intestinal polypeptide (VIP) is associated with increased mucosal cAMP levels, without a change in PGE2 release, and is unaffected by indomethacin and ketanserin. These results suggest that CT stimulates the release of 5-HT, which in turn causes the release of PGE2. The latter substances probably act via a local intramural reflex and contribute to secretion by mechanisms that are independent of cAMP.

Animals↗
PubMed1979

Importance of the intestinal inflammatory reaction in salmonella-mediated intestinal secretion.

The ability of Salmonella typhimurium to invade the intestinal epithelium is essential to the pathogenesis of salmonella-induced intestinal secretion. This invasion is accompanied by an intense acute inflammatory reaction. The present study tests the hypothesis that the acute inflammatory reaction may have a role in the pathogenesis of salmonella-induced secretion. Two groups of rabbits infected with S. typhimurium were studied: normal animals and animals pretreated with nitrogen mustard. Nitrogen mustard depletes the polymorphonuclear leukocyte pool and thereby prevents the formation of an acute inflammatory reaction. In vivo ligated ileal loops were constructed and infected 72 h after nitrogen mustard administration when polymorphonuclear leukocytes were undetectable. Nitrogen mustard treatment markedly inhibited salmonella-induced secretion. Ileal histology in normal animals infected with S. typhimurium revealed an intense acute inflammatory reaction, while in animals pretreated with nitrogen mustard only a rare polymorphonuclear leukocyte was seen. The antisecretory effect of nitrogen mustard was not merely a nonspecific effect since nitrogen mustard treatment did not inhibit cholera toxin-induced secretion and did not alter either ileal morphology nor the activities of various intestinal enzymes in normal animals. Nitrogen mustard also did not alter the virulence of the inoculated S. typhimurium. These data suggest that the mucosal inflammatory reaction induced by salmonella invasion may be important to the pathogenesis of the salmonella secretory process. The mechanism by which the inflammatory reaction stimulates secretion is not known.

Animals↗
PubMed1999

Intestinal secretion of intravenous talinolol is inhibited by luminal R-verapamil.

OBJECTIVE: To examine the secretion of the beta1-adrenergic receptor antagonist talinolol into the small intestine during its intravenous administration and to show the relevance of the P-glycoprotein-modulating drug verapamil for this secretory transport mechanism in humans. METHODS: In six healthy volunteers the intestinal steady-state perfusion technique (triple lumen tubing system) was used for measuring the appearance of talinolol within the small intestine while the drug was infused intravenously. During four of the seven perfusions performed, the perfusion fluid was changed from a verapamil-free solution and talinolol appearance was measured while a R-verapamil-containing solution (565 micromol/L) was perfused. RESULTS: Talinolol was transported into the intestinal lumen up to a concentration gradient between lumen and blood of about 5.5:1. While perfusing the small intestine with a verapamil-free solution, the intestinal secretion rate of talinolol ranged from 1.94 to 6.62 microg/min per 30 cm length of the intestine (median values). Perfusion of a R-verapamil-containing perfusion fluid resulted in lower secretion rates (0.59 to 3.71 microg/30 cm x min), corresponding to 29% to 56% of the values obtained without verapamil supplied intraluminally. CONCLUSION: Intravenously administered talinolol is actively secreted into the human small intestine. This secretion is reduced by the intraluminal supply of the P-glycoprotein modulating drug R-verapamil. This gives further rationale for P-glycoprotein-mediated intestinal drug secretion as a cause for incomplete oral bioavailability and for drug interactions during intestinal absorption.

Adrenergic beta-Antagonists↗
PubMed1979

Ionic composition of small intestinal secretion induced by PGE2.

Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions.

Animals↗
PubMed1985

[Electron microscopic research on the mechanism of intestinal secretion].

Electron microscopic investigation of the rat small intestine revealed a great number of vesicles 50-75 nm in diameter with enterocyte microvilli. The number of vesicles increased with the increase of digestive activity in the small intestine. Vesicles were formed by gemmation of enterocyte microvilli from the lateral membrane in contraction of microvillous actin skeleton. Simultaneously with the production of exocytotic vesicles, the formation of pinocytotic vesicles in the base of microvilli was observed. There is a supposition that the vesicle gemmation is a natural process of the intestinal secretion to fulfil numerous important function: it promotes the penetration of enterocyte hydrolases into the parietal layer; equilibrates an increase in the enterocyte volume during absorption. This is a possible way of translocation of synthesized enzymes into the cytoplasm and of transport proteins on the apical surface of epithelial cells.

Alkaline Phosphatase↗
PubMed1989

IgG in murine intestinal secretions. Aging effect and possible physiological role.

To assess the role of, and age-associated alterations in, intraluminal IgG in the intestine, total IgG and subclass distribution in small intestinal perfusates and pilocarpine-stimulated intestinal secretions were measured under non-fasting conditions in three groups of BALB/c mice: 2-3, 12-14, and over 24 months old. Total intraluminal IgG and its subclasses (i.e. IgG1, IgG2a, and IgG2b) increased with age. However, the binding capacities of natural intraluminal IgG antibody (Ab) for outer membrane antigen (Ag) from normal habitant bacteria (Escherichia coli and Enterobacter agglomerans) were markedly reduced in the aged lavage samples as compared with such binding in samples from the other two age groups. The striking similarity to serum in the magnitude of the increase of intraluminal IgG and also in the distribution patterns of its subclasses in the small intestinal perfusates from all age groups suggests that the serum is a major source of the IgG. The intraluminal IgG may play some role in humoral immune protection under physiologic conditions of the gut lumen.

Aging↗
PubMed1975

Effects of indomethacin on intestinal secretion, prostaglandin E and cyclic AMP: evidence against a role for prostaglandins in cholera toxin-induced secretion.

The effects of indomethacin on intestine mucosal cAMP, intestinal fluid secretion, and mucosal and fluid PGE were studied in rabbits in vivo following challenge with cholera toxin. Indomethacin had no effect on cholera toxin-induced fluid secretion or cAMP accumulation. Inhibition of PGE synthesis was achieved by the administration of two but not one injection of indomethacin. These studies provide evidence against a role for PGE in mediating cholera toxin-induced secretion and point out the need to measure prostaglandin levels when using prostaglandin synthetase inhibitors in vivo.

Animals↗
PubMed1995

Secretory monoclonal IgA class-switch variants against bacterial enteric pathogens in bile and intestinal secretions.

In a previous study we analyzed the molecular forms of monoclonal IgA class-switch variants (moIgA variants) and their transport into murine respiratory secretions. The aim of the present study is to characterize the transport of moIgA variants into bile and intestinal secretions so that their applicability in a passive immunization model of the gut can be evaluated. Different moIgA variants were directly isolated from IgG1 and IgG2a producing hybridoma clones specific for the same surface determinants of bacterial enteric pathogens (Salmonella typhimurium and Campylobacter jejuni) as their respective parent IgG clones. Hepatobiliary transport experiments clearly revealed the selective transport of biologically active polymeric forms of the IgA variants into the murine and rat bile after intravenous injection. Biotinylation of polymeric IgA variants prior to intravenous injection resulted in the recovery of functional, labeled SIgA. Moreover biotin-labeled polymeric IgA variant was recovered in bile with an increased molecular weight, suggesting that the secretory component had been added during passage through the liver. When IgA variant and IgG parent clones were both used in a murine backpack tumor model for passive immunization, IgA variant was selectively transported into intestinal secretions in comparison to IgG. The experimental model described here is suitable for use in comparative studies on the role of IgA and IgG with identical specificity in invasive infections of the intestinal tract.

Animals↗
PubMed1979

Failure to reverse cholera toxin induced intestinal secretion by agents which decrease mucosal cAMP.

The feasibility of reducing intestinal secretion by the use of agents which decrease intestinal mucosal cAMP concentration has been investigated in the weanling pig and the rabbit. Three different agents for decreasing mucosal cAMP concentration were studied. The cyclic nucleotide phosphodiesterase activator, imidazole, significantly reduced mucosal cAMP concentrations only in the weanling pig. Intraluminal 2'-deoxyadenosine-3'AMP inhibited adenylate cyclase and caused a decrease in mucosal cAMP concentration in both the pig and the rabbit. The introduction of the heat-stable enterotoxin of Escherichia coli into pig jejunal segments also gave lowered mucosal cAMP concentrations. While these three agents effectively reduced cAMP concentrations in intestinal mucosa, they were ineffective in reducing the net fluid secretory effects of cholera toxin. Secretion caused by cholera toxin apparently persists independent of the temporary changes in cAMP concentration which can be induced by pharmacological agents.

Adenylyl Cyclases↗