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Results for “INTESTINAL SECRETIONS”

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At least 415 records · Page 23Linked to original sources
PubMed1978

The effect of cholera toxin and heat labile and heat stable Escherichia coli enterotoxin on cyclic AMP concentrations in small intestinal mucosa of pig and rabbit.

The effect of cholera toxin, heat labile and heat stable Escherichia coli enterotoxin on mucosal cyclic AMP concentrations was determined on the proximal jejunum of weanling pigs and young rabbits. Ligated loops were injected with solutions containing no enterotoxin for control and either cholera toxin, heat labile or heat stable E. coli enterotoxin. The loops were drained after either two, four or six hours incubation at which time accumulated fluid was recorded and mucosal samples removed for determination of cyclic AMP concentration. In the rabbit, cholera toxin and heat labile, but not heat stable E. coli enterotoxin stimulated intestinal secretion while in the pig all three enterotoxins induced net fluid accumulation. Cholera toxin and heat labile, but not heat stable E. coli enterotoxin elevated rabbit mucosal cyclic AMP concentrations. In the pig these enterotoxins had no significant effect on mucosal cyclic AMP concentrations. The results are inconsistent with the hypothesis that the adenyl cyclase system is an essential step for enterotoxin induced intestinal secretion. The activation of intestinal adenyl cyclase by bacterial enterotoxins may only be an associated and not a necessary event for the stimulation of intestinal secretion.

Animals↗
PubMedDate not supplied

[Antitryptic and antichymotryptic activity of salivary gland secretions and intestinal contents of the medical leech Hirudo medicinalis].

Antithrombin, antitryptic and antichymotryptic activities were studied in various tissues of medical leech Hirudo medicinalis. Maximal antithrombin and antitryptic activities were found in secretion products of salivary glands. Intestinal chyme exhibited distinct antichymotryptic activity. The antichymotrypsin activity correlated with antithrombin activity in hirudin preparations, obtained after isoelectrofocusing and free of bdellines. A preparation of "pseudohirudin" exhibited neither antitryptic nor antichymotryptic activities.

Animals↗
PubMed1989

Bombesin: an activator of specific Aeromonas antibody secretion in rat intestine.

The effect of bombesin (BBS) in modulating the secretion of specific Aeromonas antibodies in rat intestine was determined. Rats were immunized with the culture supernatant of Aeromonas hydrophila, isolate SSU. This culture supernatant contained a number of toxins that may be considered virulence factors. After 24 days of immunization, rats were anesthetized and a 10-cm intestinal segment was perfused with phosphate-buffered saline. The effluents were collected for measurement of IgA and IgG by the enzyme-linked immunosorbent assay. When compared with the effect of intravenous administration of normal saline in the control group, intravenous injection of BBS (20 micrograms/kg) in the experimental group caused a significant increase in rat intestinal IgA and IgG in perfusates. The stimulatory effects of BBS on the presence of IgA and IgG were depressed partially by proglumide, a receptor antagonist of cholecystokinin (CCK) and gastrin. Treatment with pentagastrin (250 micrograms/kg) accelerated intestinal secretion of IgA, but failed to stimulate intestinal IgG secretion. In addition, intravenous injection of CCK-8 (120 ng/kg) evoked the intestinal secretion of either IgA or IgG. These findings demonstrated that BBS, gastrin, and CCK can stimulate antibody secretion in rat intestine and the stimulatory effect of BBS may be mediated partially via release of CCK and gastrin. These results suggest that neuropeptides such as BBS and gastrointestinal hormones, eg, CCK and gastrin, may participate in the regulation of intestinal secretion of IgA and IgG antibodies, respectively, in rats.

Aeromonas↗
PubMed1985

The effects of feeding either roughage or concentrate diets on salivary phosphorus secretion, net intestinal phosphorus absorption and urinary phosphorus excretion in the sheep.

Mature sheep fitted with rumen and duodenal cannulae were fed either a hay or a concentrate diet and the effects on salivary phosphorus secretion, net intestinal phosphorous absorption and pathway for phosphorous excretion were examined. Route of excretion was markedly affected by diet with urine phosphorus levels being much higher and faecal levels lower when the concentrate diet was fed. This difference was not due to differences in phosphorus intake nor could it be related to differences in either plasma phosphorus levels or net intestinal phosphorus absorption. Salivary phosphorus secretion and renal tubular reabsorptive efficiency for phosphorus were, however, both lower when the concentrate diet was fed. The significance of these effects of diet in relation to the control of phosphorus balance in ruminants is discussed.

Animal Feed↗
PubMed1976

The Syrian hamster: a reproducible model for studying changes in intestinal fluid secretion in response to enterotoxin challenge.

Syrian hamsters respond in a predictable and reproducible manner to intragastric administration of purified cholera enterotoxin by intraluminal accumulation of fluid in the small bowel, cecum, and proximal colon. In the majority of animals this process is self limiting, and recovery occurs with full reabsorption of intestinal fluid by 30 to 35 h. The secretory response to 75 mug of cholera toxin has been defined, and the model was utilized to study the inhibitory effects of indomethacin, polymyxin B sulfate, glucose electrolyte solutions, and colchicine. These studies demonstrate its potential usefulness as a convenient and inexpensive technique for evaluation of pharmacological agents that might inhibit intestinal fluid secretion.

Animals↗
PubMedDate not supplied

Adrenal tumour secreting vasoactive intestinal peptide and noradrenaline.

A patient with a ganglioneuroblastoma secreting both noradrenaline and vasoactive intestinal peptide is described. Their vasoactive effects are antagonistic and pre-operatively the patient was normotensive. Manipulation of the tumour provoked hypertension and after excision marked hypotension occurred which responded to the administration of metaraminol and blood. This case emphasises the need for thorough investigation of patients with amine or peptide-secreting tumours which have atypical features.

Adrenal Gland Neoplasms↗
PubMed1976

[Secretory immunoglobulins and serum antibodies after oral infection of the white mouse with Salmonella typhimurium (author's transl)].

White Mice were infected via the gastrointestinal tract with S. typhimurium. The immunoglobulin class of specific antibodies appearing in serum and intestinal secretions was determined. Specific antibodies were detected as early as 7 days after infection in the intestinal secretions, and reached maximum titers on day 21. These antibodies belonged exclusively to the IgA class. After day 21, at a time when serum antibodies had reached high titers, antibodies of the IgG class were also detectable in the gut in low levels. Specific antibodies of the IgM class could never be demonstrated in intestinal secretions. Antibody titers remained at almost constant levels over the entire test period of 92 days in those animals with Salmonella in their intestine. In animals, where Salmonella were no longer demonstrable in the gut, antibody titers decreased. Serum antibodies could first be detected 12 days after infection. They reached maximum titers between day 21 and 36. Until day 21 equal levels of IgG and IgM antibodies were found. Later on, antibodies of the IgG class predominated. In Salmonella carriers antibody titers remained on high levels over the entire test period. In animals negative for S. typhimurium in liver and spleen, antibody titers declined until the end of the test period. A new and simple method for raising a class-specific anti-mouse IgA Antiserum by immunization of rabbits with IgA from washings of the small intestine is described.

Animals↗
PubMed2001

Taurocholic acid-induced secretion in normal and cystic fibrosis mouse ileum.

Bile acids cause secretion throughout the intestinal tract and this process contributes to maintaining the fluidity of intestinal contents. In cystic fibrosis (CF) defective intestinal secretion can lead to excessive dehydration of the luminal contents and the development of clinical symptoms. This study was designed to investigate bile acid-induced secretion in mouse ileum and to determine whether this process was defective in CF. Taurocholic acid-induced secretion was monitored as a rise in short-circuit current (SCC) in ileal sheets from normal (Swiss MF1) and transgenic CF mice. Taurocholic acid increased the SCC in both intact and stripped ileal sheets from Swiss MF1 mice. This effect was due to a stimulation of electrogenic Cl- secretion as it was inhibited by Cl(-)-free conditions, serosal furosemide (frusemide), mucosal diphenylamine-2-carboxylic acid (DPC) and increased serosal K+ concentration, without being affected by reduced mucosal Na+ concentration. Taurocholic acid-induced secretion was inhibited by tetrodotoxin, indicating the involvement of a neural pathway, but this did not include capsaicin-sensitive afferent neurons or muscarinic cholinoreceptors. Mucosal mast cells also contributed to the response. Responses in tissues from transgenic wild-type mice were similar to those obtained with Swiss MF1 animals, but ilea from CF mice exhibited a lower basal SCC with significantly reduced secretory responses to acetylcholine and taurocholic acid. We concluded that taurocholic acid induces ileal secretion by a mechanism that entails activation of enteric nerves and degranulation of mucosal mast cells. Impaired bile acid-induced secretion in CF may contribute to luminal dehydration.

Animals↗
PubMed1987

Vibrio cholerae metalloproteinase degrades intestinal mucin and facilitates enterotoxin-induced secretion from rat intestine.

Mucin secretion in situ from rat intestinal loops was promoted more effectively by dialysed crude cholera filtrate than by an equivalent amount of purified enterotoxin. The filtrate could be rendered inactive by incubation with mixed gangliosides or passage through a GM1-affinity column, which indicated that the secretory action of the filtrate depended upon its enterotoxin component. In an effort to explain the greater potency of the filtrate, we established the presence of a metalloproteinase in the filtrate and demonstrated that this enzyme was capable of degrading purified rat intestinal mucin. Sufficient degradation occurred to cause a substantial decrease in viscosity (57% in 120 min). Biochemical analysis of the mucin before and after exposure to filtrate revealed a rise in the combined percentage of serine, threonine and proline (53-58%), suggesting that poorly glycosylated areas (which are less abundant in these amino acids) were being partly removed from the mucin. The carbohydrate composition was essentially unaltered. Inhibition of the filtrate metalloproteinase by Zincov and alpha 2-macroglobulin significantly (P less than 0.005) reduced the ability of cholera filtrate to degrade mucin or to stimulate mucin secretion from rat intestinal slices in vitro. Purified cholera enterotoxin added to enterotoxin-depleted filtrate was a more potent secretagogue (secretory stimulant) in intestinal loops than an equivalent amount of enterotoxin alone. We therefore propose that mucin secretion induced by cholera filtrate is caused by cholera enterotoxin, but that degradation of the protective epithelial mucus layer by a constituent metalloproteinase may assist the toxin by allowing increased access to mucosal GM1 receptor sites.

Amino Acids↗
PubMed1996

Immunisation of chickens to reduce intestinal colonisation with Campylobacter jejuni.

1. Systemic and intestinal antibody titres were measured in chickens following subcutaneous, intraperitoneal (i.p.), oral (p.o.) and combined i.p./p.o. administration of antigen, in soluble, emulsified or microparticulate form. Antigens tested included keyhole limpet haemocyanin (KLH), killed Campylobacter jejuni whole cells and purified campylobacter flagellin protein. 2. The effect of immunisation with purified flagellin protein or with killed C. jejuni whole cells in reducing intestinal colonisation was assessed. The ability of newlyhatched chicks to respond to immunisation was limited, possibly because of the immaturity of the immune system rather than maternal suppression of an immune response. Only 5 to 13 birds that were first immunised when 1-d-old with KLH showed a systemic response, even after 4 immunisations, whereas 10 of 11 birds that were first immunised at 24 d-old responded systemically. 3. In an immunisation and challenge experiment, birds that were immunised twice intraperitoneally, at 16 and 29 d-old, with killed C. jejuni whole cells, had fewer C. jejuni, in the caecal contents than unimmunised control birds. This reduction in intestinal colonisation, to less than 2% of bacterial numbers in control birds, was associated with an increase in specific IgG in intestinal secretions. There was no significant increase in specific IgA or IgM in intestinal secretions following immunisation and challenge. 4. These results indicate that immunisation can reduce the level of intestinal infection with C. jejuni. The protection may be enhanced by developing improved methods of immunisation that stimulate production of increased titres of specific antibody in intestinal secretions, particularly specific IgA antibody.

Animals↗
PubMed1987

The effects of feeding either hay or grass diets on salivary phosphorus secretion, net intestinal phosphorus absorption and on the partition of phosphorus excretion between urine and faeces in the sheep.

Mature sheep fitted with ruminal and duodenal cannulas were fed either a pelleted hay or a pelleted grass diet with or without supplementary phosphorus. Salivary phosphorus secretion, net intestinal phosphorus absorption and the route of phosphorus excretion were determined. The route of excretion was markedly affected by diet with urinary excretion being much higher and faecal excretion lower when the grass diet was fed. These effects were not due to differences in phosphorus intake or to differences in net intestinal phosphorus absorption. Salivary phosphorus secretion was, however, lower when the grass diet was fed. The significance of these changes in relation to the control of phosphorus balance in ruminants is discussed.

Animal Feed↗
PubMed1977

Feedback regulation of pancreatic enzyme secretion by intestinal trypsin in man.

In a patient a papilla Vateri tumor completely prevented the bile-pancreatic flow into the intestine although the pancreatic juice was secreted into the bile duct via a common channel. Consequently, the bile-pancreatic juice was possible to sample via a percutaneous transhepatic cholangiography (PTC) catheter. This made it possible to study the effect of duodenal infusion of different substances on the bile-pancreatic secretion. In repeated experiments a suppression of the secretion was observed by intraduodenal trypsin as well as the patient's own bile-pancreatic juice. In the presence the bile-pancreatic juice intraduodenal trypsin inhibitor infusion caused a marked stimulation of the secretion. The results are in accordance with the hypothesis that trypsin in the upper part of the intestine exerts a negative feedback regulation of the pancreatic secretion in man.

Aged↗
PubMed1997

Calcium channels and intestinal fluid secretion: an experimental study in vivo in rats.

Several mechanisms involved in nervous secretory reflex(es) of the enteric nervous system may be dependent on the flux of calcium across the plasma membrane, which may be controlled by voltage-gated calcium channels. In this study, we investigated the importance of plasma membrane calcium channels for intestinal fluid secretion. Two types of studies were performed, in which intestinal net fluid transport in anaesthetized rats was followed with a gravimetric method. First, the effects on intestinal fluid transport of placing A23187, a calcium ionophore, in the intestinal lumen was studied. A23187 induced in a dose-dependent manner a net fluid secretion, which was abolished by giving hexamethonium (10 mg kg(-1) body wt) i.v. or placing lidocaine (1% solution) on the intestinal serosa. Nifedipine (5.75 micromol kg(-1) body wt i.v.) also abolished the fluid secretion caused by the ionophore. In the second study, the effects of various calcium channel blockers (gadolinium chloride, nifedipine, verapamil) were tested on the cholera toxin-induced secretion. It was attenuated by luminal application of gadolinium chloride (1-10 mM) or nifedipine (10-200 microM). Intravenously administered nifedipine (2.5-5.75 micromol kg(-1) body wt) abolished cholera toxin-evoked secretion dose-dependently, whereas verapamil (0.05-1 micromol kg(-1) body wt) was without consistent effect. It is concluded that the fluid secretion evoked by placing A23187 in the intestinal lumen in vivo was induced via an activation of the enteric nervous system. Cholera secretion was attenuated or abolished by calcium channel blockers of the L- or N-type.

Anesthetics, Local↗
PubMed1990

Recognition of a 30,000 MW antigen of Giardia muris trophozoites by intestinal IgA from Giardia-infected mice.

The principal aims of this work were (i) to identify the molecular weight (MW) of Giardia muris trophozoite antigens that are recognized by IgA in small intestinal secretions from G. muris-infected mice, and (ii) to determine whether mouse intestinal Giardia-specific IgA is directed against trophozoite surfaces. BALB/c mice were infected with G. muris cysts, and intestinal secretions were harvested from these mice at various times after the start of Giardia infection, and from uninfected mice. Flow cytometry showed that intestinal IgA from G. muris-infected mice, but not from uninfected mice, became bound to trophozoite surfaces in vitro. Western blotting of trophozoite proteins with mouse intestinal secretions showed that IgA from Giardia-infected mice reacted specifically with a broad protein band of approximately 30,000 MW. This finding suggests that one or more trophozoite proteins of approximately 30,000 MW are targets for intestinal antibody in mice infected with G. muris.

Animals↗
PubMed1976

Effect of histamine on intestinal fluid secretion in the dog.

Intra-arterial infusion of histamine into the small intestine caused about a onefold increase of blood flow, edema of the intestinal tissues and mesentery, and produced a copious secretion of fluid. The jejunal secretions had an ionic composition similar to that of plasma, whereas ileal secretions contained high concentrations of HCO3 with relative low concentrations of Cl. The secretions contained protein (1.5 +/- .2 g/100 ml, range 0.5-2.4) with a similar electrophoretic pattern of plasma protein. When lissamine green was present in the blood, it also appeared in the secretion to a considerable concentration. It is inferred from these findings that a major mechanism of fluid secretion by the action of histamine involves a filtration process across the mucosal epithelium by the incrreased tissue fluid pressure due to extensive capillary leak.

Animals↗
PubMed1998

PYY stimulates synthesis and secretion of intestinal apolipoprotein AIV without affecting mRNA expression.

We tested whether exogenous peptide YY (PYY) can stimulate synthesis and lymphatic secretion of intestinal apolipoprotein AIV (apo AIV). Rats with mesenteric lymph fistulas and right atrial cannulas were given continuous intravenous infusions of control vehicle or PYY at 25, 50, 75, 100, or 200 pmol . kg-1 . h-1. PYY (75-200 pmol . kg-1 . h-1) stimulated lymphatic apo AIV output from 1.5- to 3.5-fold higher than basal output. In separate experiments, PYY (100 pmol . kg-1 . h-1) produced a 60% increase in jejunal mucosal apo AIV synthesis but had no effect on mucosal apo AIV mRNA levels at doses up to 200 pmol . kg-1 . h-1. Finally, exogenous PYY infusion (100 pmol . kg-1 . h-1) produced a plasma PYY increment of 30 pM compared with an increment of 18.7 pM in response to ileal infusion of lipid. These results support the hypothesis that PYY may be an endocrine mediator of the effects of distal gut lipid on production and release of intestinal apo AIV, likely via a posttranscriptional mechanism of action.

Animals↗
PubMed2001

Intestinal bicarbonate secretion in cystic fibrosis mice.

Gene-targeted disruption of the cystic fibrosis transmembrane conductance regulator (CFTR) in mice results in an intestinal disease phenotype that is remarkably similar to bowel disease in cystic fibrosis patients. In the intestinal segment downstream from the stomach (i.e., the duodenum), CFTR plays an important role in bicarbonate secretion that protects the epithelium from acidic gastric effluent. In this report, we examine the role of CFTR in cAMP-stimulated bicarbonate secretion in the murine duodenum and the mechanisms of acid-base transport that are revealed in CFTR knockout (CF) mice. Ion substitution, channel blocker and pH stat studies comparing duodena from wild-type and CF mice indicate that CFTR mediates a HCO(3)(-) conductance across the apical membrane of the epithelium. In the presence of a favorable cell-to-lumen HCO(3)(-) gradient, the CFTR-mediated HCO(3)(-) current accounts for about 80% of stimulated HCO(3)(-) secretion. Exposure of the duodenal mucosa to acidic pH reveals another role of CFTR in facilitating HCO(3)(-) secretion via an electroneutral, 4,4'-diisothiocyanato-stilbene-2,2' disulfonic acid (DIDS) sensitive Cl(-)/HCO(3)(-) exchange process. In CF duodenum, other apical membrane acid-base transporters retain function, thereby affording limited control of transepithelial pH. Activity of a Cl(-)-dependent anion exchanger provides near-constant HCO(3)(-) secretion in CF intestine, but under basal conditions the magnitude of secretion is lessened by simultaneous activity of a Na(+)/H(+) exchanger (NHE). During cAMP stimulation of CF duodenum, a small increase in net base secretion is measured but the change results from cAMP inhibition of NHE activity rather than increased HCO(3)(-) secretion. Interestingly, a small inward current that is sensitive to the anion channel blocker, 5-nitro-2(3-phenylpropyl amino)-benzoate (NPPB), is also activated during cAMP stimulation of the CFTR-null intestine but the identity of the current is yet to be resolved. Studies to identify the proteins involved in non-CFTR mediated HCO(3)(-) secretion are on-going and potentially will provide targets to correct deficient HCO(3)(-) secretion in the CF intestine.

Animals↗