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At least 19 recordsLinked to original sources

On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion.

Intestinal secretion was produced in anesthetized cats and rats by exposing isolated intestinal segments to cholera enterotoxin. Giving, for example, tetrodotoxin, a nerve-conduction-blocking agent, or adding lidocaine, a local anesthetic agent, to the solution in the intestinal segments markedly inhibited the rate of choleraic secretion, and in most experiments a net absorption of fluid was observed. The results suggest that intramural nervous mechanisms are involved in the pathogenesis of choleraic secretion.

Anesthetics, Local↗

A lavage technique allowing repeated measurement of IgA antibody in mouse intestinal secretions.

Mouse intestinal secretions can be readily obtained without harm to the mice by administering a lavage solution to them intragastrically followed by pilocarpine intraperitoneally. These secretions are rich in proteases but this enzyme activity can be blocked by addition of a mixture of inhibitors. Both total and specific IgA antibody could be measured in these secretions using ELISA techniques. The total IgA recovered was found to vary considerably, even in the same group of mice sampled on multiple occasions. Specific IgA anti-cholera toxin antibody was easily demonstrable in the intestinal secretions of mice fed cholera toxin but not of mice fed an irrelevant antigen. Expression of the specific IgA antibody per unit of total IgA recovered is desirable in order to correct for the variable recovery of IgA.

Animals↗

Effect of salicylates on intestinal secretion in calves given (intestinal loops) Escherichia coli heat-stable enterotoxin.

The inhibitory effect of salicylates on intestinal secretion in 1- to 5-day-old calves given Escherichia coli heat-stable enterotoxin (ST)-induced intestinal fluid response was investigated. Purified ST was diluted in isotonic saline solution to obtain 1:10, 1:25, 1:50, 1:75, and 1:100 dilutions. Each dilution (1 ml) was inoculated into ligated loops in the distal part of the jejunum of each calf. Acetylsalicylic acid (aspirin) given orally (100 mg/kg) at 4 hours before ST was inoculated did not substantially alter the intestinal fluid response to ST. Sodium salicylate (IV) infusion, begun simultaneously when, or at 1 hour after, ST was inoculated, significantly (P less than 0.05) decreased fluid accumulation in those loops inoculated with ST dilutions of 1:25 or greater. The sodium and potassium concentrations of the accumulated fluid did not differ significantly between or within treatment groups. These results indicate that sodium salicylate infusion may be beneficial in treating enterotoxic colibacillosis in calves. Aspirin given orally at the dose used in the present study, would not have any beneficial effect.

Animals↗

Alpha-2 adrenergic inhibition of intestinal secretion induced by prostaglandin E1, vasoactive intestinal peptide and dibutyryl cyclic AMP in rat jejunum.

Effects of alpha adrenergic agents on intestinal secretion induced by prostaglandin E1 (PGE1), vasoactive intestinal peptide (VIP) and dibutyryl cyclic AMP (Bt2cAMP) were investigated in rat jejunum in vivo. Oxymetazoline and clonidine were more potent than epinephrine in inhibiting the PGE1-induced secretion. Methoxamine failed to inhibit the PGE1-induced secretion even with a 100-fold higher dose than that of clonidine. A high dose (1 mumol/kg) of oxymetazoline not only inhibited the PGE1- induced secretion but also enhanced net fluid absorption. Yohimbine reversed the inhibitory effect of clonidine, whereas phenoxybenzamine did not. These antagonists per se did not produce any effects on PGE1-induced secretion. Clonidine inhibited the intestinal secretion induced by VIP or Bt2cAMP, whereas methoxamine did not. The inhibitory effect of clonidine was reversed by yohimbine. Phenoxybenzamine per se inhibited intestinal secretion induced by either VIP or Bt2cAMP. Clonidine did not produce any significant effects on PGE1- augmented cAMP levels in jejunal mucosa in vivo. These results suggest that stimulation of alpha-2 adrenoceptors in rat jejunal mucosa inhibits some mechanisms distal to cAMP generation and in turn results in the inhibition of net water intestinal secretion. These findings also raise the question of general validity of a hypothesis that alpha-2 adrenoceptors regulate cellular functions through the inhibition of adenylate cyclase activity.

Adrenergic alpha-Agonists↗

Neurotransmitters in neuronal reflexes regulating intestinal secretion.

The intestinal crypt cell secretes chloride into the lumen, resulting in accumulation of fluid that normally thins out mucus or, at higher secretory rates, flushes out the contents. The regulation of chloride secretion occurs by neural reflex pathways within the enteric nervous system. Mechanical stimulation releases 5-hydroxytryptamine (5-HT) from enterochromaffin cells with subsequent activation of intrinsic primary afferents that carry electrical signals to submucosal ganglia. After processing, interneurons activate cholinergic and vasoactive intestinal peptide (VIP) secretomotor neurons. Acetylcholine and VIP bind to epithelial receptors and stimulate sodium chloride and fluid secretion. Reflex-evoked secretory rates can be modulated by a variety of mediators at the level of the enterochromaffin cells, neurons within the reflex pathway, or epithelial cells. Understanding the complex regulatory mechanisms for chloride secretion is likely to provide mechanistic insights into constipation and diarrhea.

Animals↗

[Water and electrolytes intestinal secretion (author's transl)].

This paper reviews methods used for studying intestinal secretion in man and animals, fasting and post prandial intestinal secretion, as well as that induced by bacterial enterotoxins, hormonal stimuli, some endocrine tumours and various intraluminary agents; finally the possible mechanisms and sites of intestinal secretion are discussed. That the intestine secretes fluid under physiological conditions is not proven but seems very likely. Several mechanisms seem to be involved in the production of fluid by the intestine. The adenylate-cyclase-cyclic adenosine monophosphate (AMPc) system is currently thought to play a major role in endotoxins and some hormone-induced secretions. The site of intestinal secretion remains a matter of discussion: both crypts and villi seem to participate in the secretory process.

Adenylyl Cyclases↗

A method of obtaining, processing, and analyzing human intestinal secretions for antibody content.

Human intestinal secretions can be readily obtained using a commercially available intestinal lavage solution. Although such secretions contained abundant protease activity, significant loss of immunoglobulins was prevented by the addition of a mixture of protease inhibitors. The total content of IgA, IgM, and IgG antibody in secretions was measured using sandwich ELISA. In the secretions of ten normal volunteers IgA was most abundant (197 micrograms/ml +/- 103 SD) followed by IgM (12.5 micrograms/ml +/- 6.8 SD) and IgG (0.24 micrograms/ml +/- 0.04 SD). The IgA in secretions was predominantly secretory IgA as shown by sucrose density centrifugation. The effect of intestinal secretions on the sensitivity of the antigen-specific ELISA was tested by adding murine myeloma IgA anti-TNP added to samples of human secretions. IgA anti-TNP activity could be detected as low as 1 ng/ml, and there was no evidence of interference with the ELISA by other constituents in the secretions. Using these methods an antigen-specific secretory IgA anti-cholera toxin B subunit response in the secretions of volunteers given an oral B subunit vaccine was readily demonstrated.

Antibodies↗

Intestinal secretion induced by vasoactive intestinal polypeptide. A comparison with cholera toxin in the canine jejunum in vivo.

The effect of vasoactive intestinal polypeptide (VIP) on intestinal water and electrolyte transport and transmucosal potential difference was investigated in the dog jejunum in vivo and compared to secretion induced by cholera toxin. Isolated jejunal loops were perfused with a plasma-like electrolyte solution. VIP (0.08 mug/kg per min) was administered directly into the superior mesenteric artery by continuous infusion over 1 h. From a dye dilution method, it was estimated that a mean plasma VIP concentration of 12,460 pg/ml reached the loops. VIP caused secretion of water and electrolytes; for example, chloride: control, 8 mueq/cm per h absorption; VIP, 92 mueq/cm per h secretion. A marked increase in transmucosal potential difference (control, -1.0 mV; VIP, -5.9 mV, lumen negative) occurred within 1 min after starting VIP infusion. Analysis of unidirectional fluxes showed increased plasma-to-lumen flux of sodium and chloride and decreased lumen-to-plasma flux of sodium. Chloride and bicarbonate were actively secreted against an electrochemical gradient. Although sodium secretion occurred down an electrochemical gradient, flux ratio analysis suggested a component of active sodium secretion. VIP caused a slight increase in protein output into the loops; light microscopy revealed capillary dilatation and closed intercellular spaces. The effect of VIP was readily reversible. Except for the delayed onset of secretion, the effect of cholera toxin was qualitatively similar to VIP; however, capillary dilatation and increased protein output were not noted with cholera toxin.

Animals↗

Effect of secoverine and atropine on intestinal secretion and motor activity in the rat small intestine in-vivo.

The actions of secoverine and atropine on bethanechol-induced intestinal secretion, hypermotility and transintestinal potential difference were investigated in the rat jejunum in-vivo. Both secoverine (10(-7) mol kg-1) and atropine (1.2 X 10(-9) mol kg-1) inhibited motility at doses that did not affect secretion or transintestinal potential difference. However, secoverine was a less potent antagonist of all the bethanechol-induced changes than atropine. Increases in transintestinal potential difference were more closely related to production of fluid secretion than to increases in motility.

Animals↗

Enzyme-linked immunosorbent assay for Giardia-specific IgA in mouse intestinal secretions.

We describe an ELISA for trophozoite-specific IgA in the intestinal secretions of mice infected with Giardia muris. Using this method, trophozoite-specific IgA was demonstrated in intestinal secretions of Giardia-infected immunocompetent BALB/c mice. Such antibody was undetectable in the intestinal secretions of Giardia-infected athymic (nude) mice. Immunocompetent BALB/c mice are able to clear G. muris infection whereas nude mice are not. The study provides evidence that the chronicity of G. muris infection in nude mice results from lack of intestinal trophozoite-specific IgA in these animals. By means of the ELISA, trophozoite-specific IgA was demonstrated in intestinal secretions from immunocompetent mice in the absence of protease inhibitors.

Animals↗

Mucosal protection through active intestinal secretion: neural and paracrine modulation by 5-hydroxytryptamine.

5-Hydroxytryptamine (5-HT) is widely distributed within enteroendocrine cells and neurons of the digestive tract. It stimulates active anion secretion in the intestinal epithelium, an effect which promotes the dilution and elimination of luminal pathogens. The intestinal secretory effects of 5-HT appear to be mediated in part by epithelial 5-HT2 like receptors that are linked to phosphatidylinositol turnover. In addition, 5-HT appears to interact with 5-HT3 or 5-HT4 receptors on submucosal neurons to elicit neuronal depolarization and an associated increase in intestinal secretion. Although the precise cellular mechanisms by which 5-HT modulates mucosal ion transport are incompletely understood, it is clear that 5-HT plays an important role as a intestinal secretagogue in certain diarrheal states, in laxation, and in intestinal hypersensitivity reactions.

Animals↗