Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INTESTINAL SECRETIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed1992

Indomethacin decreases jejunal fluid secretion in addition to luminal release of prostaglandin E2 in patients with acute cholera.

Human cholera is associated with an increased luminal release of prostaglandin E2 (PGE2), but whether inhibition of increased PGE2 synthesis will reduce or control intestinal secretion is uncertain. 'Steady state' perfusions (10 ml/minute) in 12 patients with acute cholera, and repeat perfusions in nine of these patients during the convalescent phase were therefore performed using the triple lumen technique. The proximal jejunum was perfused with isotonic saline containing sodium-sulphobromophthalein as a non-absorbable marker. After intravenous administration of indomethacin (1.0 mg/kg) the jejunal net transfer of fluid and the jejunal flow rate of PGE2 were determined in 30 minute periods for 120 minutes after a 120 minute control period. Indomethacin decreased net fluid secretion (2.1 (0.3-4.2) v 4.5 (2.5-8.4) ml/hour x cm; medians, Q50 ranges, p less than 0.01) and the jejunal flow rate of PGE2 (1.5 (1.2-2.7) v 2.2 (1.4-4.9) ng/minute, p less than 0.05). The results of similar perfusion studies in 22 patients with acute cholera, used to establish the spontaneous time related change in fluid secretion, showed no significant change in net fluid transfer (3.5 (2.2-6.2) to 3.5 (2.6-11.6) ml/hour x cm, p greater than 0.25) over 240 minutes. These data provide further evidence in favour of the hypothesis that prostaglandins have a role in the cholera toxin induced intestinal fluid secretion in man.

Adult↗
PubMed1991

Manipulation of intestinal immune responses against ovalbumin by cholera toxin and its B subunit in mice.

We studied the effect of mucosal presentation of ovalbumin (OVA) conjugated to cholera toxin (CT) or cholera toxin B subunit (CTB) on the intestinal immune responses against OVA. Mice were primed intraperitoneally (i.p.) with OVA in a water-in-oil emulsion and boosted intraduodenally (i.d.) with OVA conjugated to CT or CTB in various molar ratios. Responses were evaluated by testing intestinal secretions for OVA-specific antibodies and by quantifying the OVA-specific antibody secreting cells (ASC) in the lamina propria of the small intestine. OVA-CT conjugates were tested in a molar ratio ranging from 1.8:1 to 4500:1. OVA-CTB conjugates were tested in a molar ratio ranging from 0.25:1 to 500:1. The optimum intestinal immune response was reached at a molar ratio of 1.8:1 for OVA-CT and 5:1 for OVA-CTB. The binding capacity of OVA-CTB, but not of OVA-CT, to GM1 ganglioside corresponded with the capacity to enhance the intestinal immune response. The effect of conjugating CTB or CT to OVA on the immune response against OVA was more striking when mice were not only boosted i.d., but also primed i.d. Both OVA-CT and OVA-CTB induced detectable immune responses, whereas free OVA did not. Therefore, the carrier effect of CT or CTB is essential to trigger a mucosal immune response against OVA when presented mucosally only. We conclude that enhancing antigen uptake greatly facilitates mucosal immune responses.

Adjuvants, Immunologic↗
PubMed1978

Effect of heat stable and heat labile Escherichia coli enterotoxins and cholera toxin in combination with theophylline on unidirectional sodium and chloride flux in the small intestine of weanling swine.

The effect of heat stable and heat labile Escherichia coli enterotoxins or cholera toxin in combination with theophylline on net water, sodium and chloride and unidirectional sodium and chloride fluxes was examined in acute isolated loops of jejunum of weanling swine. The effect of heat stable enterotoxin in combination with theophylline was determined in loops located in the proximal jejunum, while combinations of theophylline and either heat labile enterotoxin or cholera toxin were studied in the distal jejunum. In each situation the addition of theophylline resulted in an additive rather than a synergistic increment of intestinal secretory activity. This study implies that the intestinal adenyl cyclase system and enterotoxin induced intestinal secretion may not be directly related in the swine small intestine.

Animals↗
PubMed1984

The involvement of calcium in the intestinal response to secretagogues in the rat.

The involvement of Ca2+ in the regulation of intestinal secretion was investigated in stripped sheets of rat mid-intestine. Removal of serosal Ca2+ together with the addition of EGTA at concentrations of 0.5 and 1 mM inhibited the rise in short-circuit current (s.c.c.) induced by both acetylcholine and theophylline, a similar degree of inhibition being observed with both secretagogues. Ca2+-free serosal fluid with 0.5 mM-EGTA added reduced significantly the rises in s.c.c. induced by A23187, acetylcholine, 5-hydroxytryptamine, theophylline, dibutyryl cyclic AMP and prostaglandin E2, but not the increased s.c.c. associated with glucose absorption. The Ca2+ channel blocker verapamil produced similar results. The calmodulin antagonist trifluoperazine inhibited secretagogue action while its sulphoxide derivative was without effect at the same concentration. The intracellular Ca2+ antagonist TMB-8 reduced the increased s.c.c. observed with acetylcholine and dibutyryl cyclic AMP. The net Cl- secretion, but not the decreased mucosal-to-serosal Na+ flux, induced by acetylcholine was abolished in Ca2+-free conditions. There was no consistent effect on the reduction in the residual ion flux caused by acetylcholine. Absence of Ca2+ converted the stimulation of Cl- secretion induced by dibutyryl cyclic AMP observed under control conditions to an enhancement of net Na+ and Cl- absorption. It is concluded that intestinal secretagogues, whether they act through cyclic AMP or not, require both internal and external sources of Ca2+ if they are to produce their full effects. Moreover, it appears that the nature of the response to dibutyryl cyclic AMP depends on the prevailing Ca2+ concentration.

Acetylcholine↗
PubMed1983

Infectious diarrhoea and gastrointestinal hormones: potential therapeutic implications.

The gastrointestinal hormones, which are continuously increasing in number, have certain effects which could play a part in the pathogenesis of infectious diarrhoea. This refers especially to VIP, motilin, and enteroglucagon, the plasma concentrations of which are elevated in acute infectious diarrhoea, cholera, and tropical malabsorption. They may act by stimulating intestinal secretion, inhibiting absorption, and altering intestinal motility. In addition, there are some hormonal effects such as those caused by glucagon on motility, by enkephalins on secretion, and by somatostatin on both, which have a therapeutic potential and deserve further investigation.

Bacterial Infections↗
PubMed1991

Antisecretory effect of splanchnic nerve stimulation on choleratoxin-induced secretion in the cat, an effect mediated at the crypts.

The experiments were performed on cats anaesthetized with alpha-chloralose. Segments of the small intestine were perfused with sodium-free hypotonic choline-mannitol solution and intestinal net fluid transport was recorded with a volumetric technique. The content of sodium and chloride in the lamina propria of the small intestinal villus was measured with an electron microprobe in freeze-dried paraffin embedded tissue. In absorbing control intestine, there was an even distribution of electrolytes along the villi. Sympathetic nerve stimulation (5 Hz, 5 ms, 5 V) did not significantly affect electrolyte distribution and net fluid transport. Intestinal secretion was elicited by pretreatment of the intestine with cholera toxin. The concentration of sodium and chloride was elevated in the apical third of the villi in intestines during the secretion since secreted sodium from the crypts was reabsorbed into the villi. Sympathetic nerve stimulation decreased the cholera secretion significantly in intestines pretreated with cholera-toxin. Furthermore, the apical gradients of sodium and chloride in the villi, caused by the reabsorbed sodium and chloride, disappeared during sympathetic nerve stimulation. It is concluded that, in the used experimental model, the antisecretory effect of sympathetic nerve stimulation was caused by inhibition of crypt secretion and not by augmented villus absorption.

Animals↗
PubMed1997

Bromelain prevents secretion caused by Vibrio cholerae and Escherichia coli enterotoxins in rabbit ileum in vitro.

BACKGROUND & AIMS: Diarrhea is a major cause of illness and death in children and young animals. The aim of this study was to investigate the possible therapeutic effect of bromelain, a proteolytic extract obtained from pineapple stems on bacterial toxin and second-messenger agonist-induced intestinal secretion. METHODS: The effect of bromelain pretreatment on short-circuit responses to Escherichia coli heat-labile enterotoxin, heat-stable enterotoxin, and Vibrio cholerae cholera toxin was evaluated in rabbit ileum mounted in Ussing chambers. RESULTS: Bromelain was 62% effective in preventing heat-labile enterotoxin-induced secretion, 51% effective against cholera toxin, and 35% effective against heat-stable enterotoxin [corrected]. Bromelain also prevented secretory changes caused by prostaglandin E2, theophylline, calcium-ionophore A23187, 8-bromoadenosine 3':5'-cyclic monophosphate, and 8-bromoguanosine 3':5'-cyclic monophosphate, well-known intracellular mediators of ion secretion. The efficacy of bromelain was not caused by reduced tissue viability resulting from its proteolytic effects on enterocytes, indicated by experiments measuring uptakes of nutrients into intestinal cells and experiments measuring short-circuit responses to glucose. CONCLUSIONS: Bromelain prevents intestinal fluid secretion mediated by secretagogues that act via adenosine 3':5'-cyclic monophosphate, guanosine 3':5'-cyclic monophosphate, and calcium-dependent signaling cascades. It may be clinically useful as an antidiarrheal drug.

Animals↗
PubMed1997

Dietary diosgenin attenuates subacute intestinal inflammation associated with indomethacin in rats.

We investigated the effects of dietary diosgenin (Dio), a plant-derived sapogenin, on indomethacin (Indo)-induced intestinal inflammation and alterations in bile secretion in rats. In anesthetized rats, bile secretion, intestinal inflammation, and blood chemistry were assessed 3 days after two subcutaneous injections of Indo given 24 h apart. Dio (> 80 mg.kg-1.day-1) pretreatment significantly inhibited weight and food intake decreases and intestinal inflammation. This protective effect was confirmed by examination of gross and histological findings and intestinal myeloperoxidase activity. Dio significantly increased biliary cholesterol (Chol) output and prevented the decreases in bile flow, bile acid output, and biliary alpha-muricholic acid and the increases in biliary hyodeoxycholic acid, deoxycholic acid, and hydrophobicity index of bile. Significantly more biliary Chol and phospholipids were present in macromolecules separate from bile acids and Indo in Dio-treated rats. Dio significantly increased the elimination constant of Indo and reduced plasma Indo levels at 3 and 12 h but did not influence biliary secretion of Indo for 3.5 h after injection. Although Dio dose-dependently attenuated subacute intestinal inflammation and normalized bile secretion in this model, it may also compromise the anti-inflammatory action of indo.

Acute Disease↗
PubMed1978

Effect of modified sham feeding on jejunal transport and pancreatic and biliary secretion in man.

Because previous evidence suggested that intestinal secretion was under parasympathetic control, we investigated the effect of modified sham feeding on the intestinal transport of water and electrolytes by jejunal perfusion using a triple lumen tube. By measuring the concentration of amylase, protein, and bile acids entering the intestinal test segment, we were also able to obtain data on the influence of sham feeding on pancreatic and biliary secretion. Gastric contents were aspirated throughout the experiment. Although we observed a clear-cut cephalic phase of gastric acid secretion, sham feeding had no effect on jejunal transport of water and electrolytes or on the rate at which bile acids, protein, or amylase were secreted into the duodenum.

Adult↗
PubMed1990

Histamine augments colonic secretion in guinea pig distal colon.

We tested the hypothesis that the role of histamine in the control of intestinal secretion is mediated by prostaglandins (PGs). The effects of histamine on ion transport were examined in muscle-stripped sheets of mucosa/submucosa set up in flux chambers. Histamine evoked a transient concentration-dependent increase in short-circuit current (Isc) that was reduced by the Cl- transport inhibitor bumetanide. Histamine also caused the release of PGE2. The Isc response to histamine was reduced by indomethacin and piroxicam, which block PG formation, but not by nordihydroguaiaretic acid, which prevents production of lipoxygenase products. 2-Methylhistamine, but not dimaprit, evoked a concentration-dependent increase in Isc. The Isc response to histamine was reduced by the H1-blocker pyrilamine, but not by the H2-antagonist cimetidine. In addition to its direct effect, histamine augmented the responses of endogenously released neurotransmitters with and without indomethacin and hexamethonium. Tetrodotoxin (TTX) reduced the Isc response to 10(-3) M histamine. In the presence of TTX, exogenous histamine amplified the responses to PGs, vasoactive intestinal polypeptide, 2-chloroadenosine, bethanechol, and carbachol. These results suggest that histamine acts at H1-receptors on cells within the gut to mediate intestinal Cl- secretion in part by releasing PGs and by augmenting the actions of endogenously released neurotransmitters. Our results indicate that histamine has a role in the regulation of colonic transport function.

2-Chloroadenosine↗
PubMed2000

Why should a clinician care about the molecular biology of transport?

This review outlines the progress made over the last few years in three chosen areas of intestinal ion transport. In the field of intestinal secretion, research on the secretion of bicarbonate by pancreatic ducts and duodenal epithelia in cystic fibrosis revealed the crucial role of chloride channel (CFTR) in the control of activity of other transporters involved in bicarbonate secretion. In the area of intestinal absorption, studies on the regulation and physiologic roles of epithelial Na(+)/H(+) exchangers confirmed the suspected involvement of recycling in the acute regulation of NHE3 activity and resulted in formulation of new concepts for the roles of NHE3 and NHE2 in the gastrointestinal tract. Finally, the recent discovery of the first known viral enterotoxin revolutionized our understanding of pathomechanisms of secretory diarrhea during viral infections in humans. All of these findings are discussed in the context of their utility to the practicing gastroenterologist.

Biological Transport↗
PubMed1988

Effect of acute Yersinia enterocolitica infection on in vivo and in vitro small intestinal solute and fluid absorption in the rabbit.

The impact of acute Yersinia enterocolitica infection on jejunal and ileal solute and water transport was examined. New Zealand White rabbits (500-600 g) were infected with Y. enterocolitica and compared with unmanipulated controls and pair-fed controls. Transport studies were performed 6 days after infection on jejunum and ileum by an in vivo single-pass perfusion technique and in vitro under short-circuited conditions in Ussing chambers. When studied in vivo, Y. enterocolitica infection resulted in decreased water and electrolyte absorption in the jejunum under basal conditions and in both jejunum and ileum in the presence of glucose. Glucose absorption was also decreased in jejunum and ileum. When studied in vitro, net basal Na+ and Cl- transport was not altered in jejunal or ileal epithelium from infected animals. Glucose-stimulated Na+ absorption was decreased in ileal epithelium, and absorption of 3-O-methyl-D-glucose was decreased in both jejunum and ileum. Secretory capacity of Cl-, as assessed by isobutylmethyl xanthine stimulation, was unimpaired in both jejunum and ileum. Decreased food intake alone, in the pair-fed animals, had little effect on intestinal transport. The results indicate that malabsorption, rather than active intestinal secretion, is the major small intestinal transport defect in acute Y. enterocolitica infection. Furthermore, the abnormalities can be directly attributed to injury induced by the organism itself, rather than malnutrition.

Acute Disease↗
PubMed1998

Antidiarrheal agents for the management of treatment-related diarrhea in cancer patients.

The efficacy and use of antidiarrheal agents in patients who diarrhea associated with cancer treatments are reviewed. Diarrhea is common in cancer patients and may interfere with cancer treatment. Diarrhea may be induced by chemotherapy, radiation therapy, surgery, graft-versus-hot disease (GVHD) or infection after bone marrow transplantation, and other causes. The general goal of antidiarrheal therapy is to reduce fluid loss in the stool by inhibiting intestinal secretion, promoting absorption, and decreasing intestinal motility. Antidiarrheal agents may be classified as intestinal transit inhibitors, intraluminal agents, proabsorptive agents, and antisecretory drugs. Opiate agonists are the most commonly used intestinal transit inhibitors; they can be effective in treating cancer treatment-related diarrheas but must be used cautiously. Intraluminal agents include clays, activated charcoal, and cholestyramine; these adsorbents and other binding resins can interfere with the absorption of orally administered antidiarrheals and other drugs and are unlikely candidates for use in most cases of diarrhea in cancer patients. Clonidine, a proabsorptive agent, should be used only in patients with secretory diarrhea refractory to opiate agonist treatment. Octreotide is an antisecretory drug that has shown considerable efficacy in clinical trails as a treatment for diarrhea caused by chemotherapy of GVHD; its use for radiation therapy-induced diarrhea, although not studied clinically, is nevertheless an option. In general, opiate agonists and octreotide appears to offer the most efficacy and flexibility. Opiate agonists and octreotide are effective agents for cancer treatment-related diarrhea.

Antidiarrheals↗
PubMed1990

[Secretory humoral immunity in children with chronic viral diseases of the liver].

The content of IgE, IgG, IgM and secretory IgA was measured in the stomatopharyngeal secretion (saliva) and in the intestinal secretion (coprofiltrates) of 58 patients aged 3 to 15 years suffering from chronic viral hepatitis and liver cirrhosis. It has been established that in addition to hyperimmunoglobulinemia, children with chronic viral diseases of the liver manifested elevated synthesis of immunoglobulins in the system of local immunity, including a high content of IgE in the alimentary secretions, thus pointing to enhanced antigenic stimulation occurring in this pathology.

Adolescent↗
PubMed1989

[Physiologic role of the sodium pump. Implications for the study of arterial hypertension].

Mammalian cells have the same hydroelectrolytic composition (high K, low Na), highly different from that of their surrounding. Constancy of cellular composition is insured by the balance between ionic leaks and (Na, K)-pump activity. Ionic leaks, specially sodium, are fundamental. They allow cells to perform a majority of their general and special functions (import of aminoacids, glucose, phosphates; export of acids; nerve influx; muscular contraction; glandular secretion; intestinal and renal reabsorption and secretion). (Na, K)-pump is essential to life. It is a kind of general motor that creates and maintains ionic concentrations differences whose potential energy is dissipated by leaks to perform cellular functions. Constancy of hydroelectrolytic intracellular composition hides that leak and pump rates, equivalent between them, are extremely variable among cell types (more than 200 times), and can increase 4 times in less than one minute within a cell type with cellular activity. In a cell, (Na, K)-pump rate is far from maximum velocity. This rate is adjusted nearly instantaneously to balance variations in leak rates; it may undergo short term modulation by endo or exocellular factors; it may undergo long term changes through synthesis of new enzyme molecules. Studies on whole cells of the balance between leaks and pump rates is necessary to understand these cells physiology and pathology. Balance between leaks and (Na, K)-pump activity is altered in renal cells from hypertensive rats, spontaneously (SHR) or genetically selected (Milan Hypertensive Strain: MHS). Strikingly, sodium activation of (Na, K)-pump of inner medullary collecting duct cells of MHS rats is greatly blunted compared to controls.

Adenosine Triphosphatases↗
PubMed1994

Disulfide bond formation between dimeric immunoglobulin A and the polymeric immunoglobulin receptor during hepatic transcytosis.

The polymeric immunoglobulin receptor on rat hepatocytes binds dimeric IgA on the sinusoidal surface and mediates its transport to the canaliculus, where the complex of dimeric IgA and secretory component, the cleaved extracellular domain of polymeric immunoglobulin receptor, is secreted into bile. This process is unique in that disulfide bonds are formed between dimeric IgA and polymeric immunoglobulin receptor during transcytosis, permanently preventing their dissociation. Here we present three lines of evidence that disulfide bonding between dimeric IgA and polymeric immunoglobulin receptor occurs predominantly in a late transcytotic compartment and that hepatic transcytosis can proceed in the absence of disulfide bond formation. First, throughout the course of transcytosis the percentage of intracellular dimeric IgA disulfide bonded to polymeric immunoglobulin receptor is less than half that in bile, suggesting that disulfide bond formation is a late event in transcytosis. Second, dimeric IgA that recycles from early endocytotic compartments into the circulation is mostly noncovalently bound to secretory component. Finally, the rate of transcytosis of dimeric IgA and its appearance in bile are not affected when disulfide bond formation with polymeric immunoglobulin receptor is inhibited by blocking of free thiol groups on dimeric IgA with iodoacetamide. These results are consistent with other findings in the literature and indicate that the main physiological role of disulfide bond formation between dimeric IgA and polymeric immunoglobulin receptor is not to facilitate transcytosis but, rather, to stabilize the dimeric IgA-secretory component complex after its release into external secretions such as bile and intestinal secretions.

Animals↗
PubMed1999

Net secretion of furosemide is subject to indomethacin inhibition, as observed in Caco-2 monolayers and excised rat jejunum.

PURPOSE: To determine if intestinal secretion occurs for the poorly bioavailable diuretic, furosemide. METHODS: Jejunal segments of male Sprague-Dawley rats were mounted on diffusion chambers, and the permeation of furosemide was measured across the excised tissue in both directions. Studies were repeated using cultured epithelia from adenocarcinoma cells (Caco-2) grown on filter inserts mounted in 6-well plates. Temperature-dependence and chemical inhibition by indomethacin was also tested using the cell culture model. RESULTS: Net secretion from rat intestine of over 3-fold was observed for 20 microM furosemide. Net secretion of furosemide by Caco-2 cells was over 300% greater than for intestinal segments (10-fold vs. 3-fold). For both models, a decrease in furosemide transport in the direction of secretion was observed in the presence of indomethacin (100 microM), although only results using the Caco-2 cells showed in increase in the absorptive transport. Furosemide secretion from Caco-2 cells decreased with decrease in temperature from 37 degrees C to 4 degrees C, suggesting a carrier-mediated process. CONCLUSIONS: Furosemide appears to be secreted in the small intestine. These preliminary results indicate that furosemide bioavailability may be limited by an intestinal transporter.

Animals↗
PubMed2003

Seirogan (wood creosote) inhibits stress-induced ion secretion in rat intestinal epithelium.

Acute stress in often associated with abnormalities in gastrointestinal function, including enhanced secretion of water and electrolytes that leads to diarrhea. The goal of our study was to investigate whether Seirogan inhibits stress-induced intestinal secretion in Wistar-Kyoto rats. Electrogenic ion secretion was measured in modified Ussing chambers as an increase in basal short-circuit current (Isc) across isolated rat jejunal or colonic mucosal sheets. Mucosal preparations from rats exposed to cold restraint stress showed a significant increase in basal Isc compared to controls. The cumulative addition of Seirogan to the Ussing chamber caused a concentration-dependent reduction of the stress-induced increase of basal Isc to levels resembling nonstressed controls. In a separate experiment, Seirogan (15 mg/kg) administered by oral gavage inhibited stress-induced secretion and normalized basal Isc in the jejunum and colon. The results suggest that Seirogan may be an effective therapy for patients with stress-associated diarrhea.

Administration, Oral↗