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Results for “INTESTINAL SECRETIONS”

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At least 577 records · Page 32Linked to original sources
PubMed1988

Reinfusion of secretions from high-output proximal stomas or fistulas.

Patients with proximal stomas or high fistulas and defunctionalized intestine who are receiving total parenteral nutrition (TPN) often develop hepatic enzyme abnormalities and hyperbilirubinemia. A technique was developed to collect intestinal secretions from proximal stoma and to reinfuse these secretions into the distal part of the intestine. This technique was applied in eight patients with a disrupted intestinal tract. A significant decrease (p less than 0.05) in elevated serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase levels was observed. Alanine aminotransferase and aspartate aminotransferase levels did not change significantly. The plasma sodium levels, slightly subnormal before reinfusion (131.0 +/- 4.6 millimolar per liter), despite enormous supplementation, normalized during reinfusion (137.0 +/- 4.0 millimolar per liter). TPN was continued during this infusion. This suggests that TPN by itself does not cause intrahepatic cholestasis. Neither could it be explained by an effect of secondary bile acids because these were most likely not produced as bile did not reach the distal defunctionalized intestine. Three possible mechanisms are suggested. Restoration of passage in the distal intestine may diminish bacterial overgrowth, endotoxin production and absorption. Enlargement of the bile acid pool may diminish the susceptibility of the liver to the deleterious effects of endotoxins. We advocate this reinfusion technique to overcome the metabolic disturbances occurring in those patients with high-output stomas or fistulas arising from the proximal parts of the small intestine.

Adult↗
PubMed2003

Enhanced mucosal immunity against Eimeria acervulina in broilers fed a Lactobacillus-based probiotic.

The effect of feeding a Lactobacillus-based probiotic on intestinal intraepithelial lymphocyte (IEL) subpopulations and subsequent protection against coccidiosis was investigated in broiler chickens. Day-old male broilers were fed standard rations without control (CONT) or with a commercial probiotic (PROB) Primalac. Differences in IEL subpopulations were assessed by flow cytometry at 21 d postprobiotic treatment. At 25 d of age, a group of randomly selected birds from each diet was inoculated orally with 10,000 (per bird) sporulated oocysts of Eimeria acervulina and kept on the same diets. Fecal material, sera, and intestinal washes were collected 10 d postchallenge with E. acervulina. Birds on the PROB diet had more IEL expressing the surface markers CD3, CD4, CD8, and alphabetaTCR than those of the CONT diet. The probiotic-fed chickens produced less oocysts (P < 0.0001) compared to the untreated, control group (368 x 10(6) in CONT vs. 89 x 10(6) in PROB). The interferon-gamma levels in both serum and intestinal secretions were not significantly different between the two groups. However, CONT group showed higher antibody levels against a recombinant coccidial antigen in the intestinal secretions than the PROB group. No significant difference was found in serum antibody levels against the same antigen. These results dearly indicate that the probiotic bacteria impacted the local immune response as characterized by altered IEL subpopulations and increased the birds' resistance to E. acervulina as reflected by reduced oocyst shedding.

Animals↗
PubMed1999

Characterization of the inhibitory effect of boiled rice on intestinal chloride secretion in guinea pig crypt cells.

BACKGROUND & AIMS: When rice is incorporated into oral rehydration therapy for patients with secretory diarrhea, clinical outcomes improve. We have shown that a factor purified from boiled rice (RF) blocks the secretory response of intestinal crypt cells to adenosine 3',5'-cyclic monophosphate (cAMP). Now we report that the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is the cellular target for this rice inhibitor. METHODS: We used RF, the same previously described extract prepared from boiled rice, to assess chloride channel activation in vitro, measuring (1) cell volume regulation of guinea pig intestinal crypt epithelial cell suspensions using standard Coulter counter technology, (2) transepithelial chloride current in monolayers of T84 cells mounted in Ussing chambers, and (3) whole-cell and single-channel currents using the patch-clamp technique in cells transfected to express CFTR. RESULTS: RF inhibited activation by cAMP of CFTR chloride channels in all experimental preparations; RF did not block volume-stimulated Cl- secretion, suggesting that its effect might be specific for CFTR chloride channels. RF inhibited transepithelial cAMP-stimulated Cl- current in T84 cells and inhibited forskolin (i.e., cAMP)-induced current in cells transfected with CFTR. Excised patch and single-channel patch-clamp recordings supported the view that the response was a direct effect on CFTR rather than on cAMP signal transduction. CONCLUSIONS: RF exerts a specific inhibitory effect on CFTR chloride channels, blocking activation from the luminal surface of the cell and reversing established activation. Many major diarrheal states are based on cAMP-induced CFTR activation, leading to excessive gut secretion; our findings could have clinical relevance.

Animals↗
PubMed1981

Clinicopathological study of pancreatic and ganglioneuroblastoma tumours secreting vasoactive intestinal polypeptide (vipomas).

During a six-year period (1973-9) 52 patients with pancreatic tumours and 10 with ganglioneuroblastomas were found to have raised plasma vasoactive intestinal polypeptide (VIP) concentrations. All the patients had severe secretory diarrhoea, weight loss, dehydration, hypokalaemic acidosis, and a raised plasma urea concentration. Reduced gastric acid secretion was seen in 72% of patients. Plasma VIP concentrations were not raised in patients with diarrhoea due to other types of tumour or disease or in hormone-secreting tumours not associated with diarrhoea. Plasma VIP measurement may therefore give clinical guidance in a patient with persistent watery diarrhoea and hypokalaemic acidosis. Surgical excision was clearly the treatment of choice, but metastatic pancreatic tumours usually responded to streptozotocin.

Adult↗
PubMed2004

Prevention of toxin-induced intestinal ion and fluid secretion by a small-molecule CFTR inhibitor.

BACKGROUND & AIMS: The cystic fibrosis transmembrane conductance regulator (CFTR) provides an important apical route for Cl(-) secretion across intestinal epithelia. A thiazolidinone-type CFTR blocker (CFTR(inh)-172) reduced cholera toxin-induced fluid accumulation in mouse intestinal loops. Here, we characterize the efficacy and pharmacodynamics of CFTR(inh)-172 in blocking cAMP and cGMP induced Cl(-)/fluid secretion in rodent and human intestine. METHODS & RESULTS: CFTR(inh)-172 inhibited cAMP and cGMP agonist induced short-circuit current by >95% in T84 colonic epithelial cells (K(I) approximately 3 micromol/L) and in mouse and human intestinal sheets (K(I) approximately 9 micromol/L). A single intraperitoneal injection of CFTR(inh)-172 (200 microg) blocked intestinal fluid secretion in a rat closed-loop model by >90% for cholera toxin and >70% for STa Escherichia coli toxin. In mice, CFTR(inh)-172 (20 microg) inhibited cholera toxin-induced intestinal fluid secretion by 90% (persistence t(1/2) approximately 10 hours, K(I) approximately 5 microg) and STa toxin by 75% (K(I) approximately 10 microg). Tissue distribution and pharmacokinetic studies indicated intestinal CFTR(inh)-172 accumulation facilitated by enterohepatic circulation. An oral CFTR(inh)-172 preparation reduced fluid secretion by >90% in a mouse open-loop cholera model. CONCLUSIONS: A small molecule CFTR blocker markedly reduced intestinal ion and fluid secretion caused by cAMP/cGMP-dependent bacterial enterotoxins. CFTR inhibition may thus reduce fluid secretion in infectious secretory diarrheas.

Administration, Oral↗
PubMed1974

Erosive gastritis with special reference to the role of aspirin and bile.

The high mortality associated with the surgical treatment of erosive gastritis is related to the postoperative continuing haemorrhage rate. Immediate gastroscopy has significantly improved preoperative diagnosis, and in 30 cases treated by the Billroth I operation continuing haemorrhage was seen on only one occasion.The frequent association of chronic gastritis and drug-associated erosive gastritis suggests that the gastritic mucosa is unusually susceptible to aspirin. Experiments designed to investigate the effect of biliary diversion on aspirin-induced gastric mucosal damage demonstrated a significant increase in such damage.Intestinal metaplasia and chronic gastritis of the gastric mucosa develop when upper intestinal secretions are diverted into the stomach either surgically or by pyloric regurgitation. Postoperative gastric aspiration indicates that the Billroth I operation is associated with far less regurgitation of upper intestinal secretions postoperatively than either the Polya operation or vagotomy and drainage. It is suggested that the efficacy of the Billroth I operation in controlling haemorrhage in the immediate postoperative period is related to this. In the long term the reduced incidence of intestinal metaplasia in the Billroth I gastric remnant reflects a minimal tendency to biliary reflux.

Acute Disease↗
PubMed1984

Generalized systemic and mucosal immunity in mice after mucosal stimulation with cholera toxin.

Cholera toxin (CT) has been found to be an extremely potent immunogen for mucosal IgA responses when administered via the intestine. This study has examined both mucosal and systemic immune responses after feeding CT and compared these responses with those obtained after feeding keyhole limpet hemocyanin (KLH), another protein that is strongly immunogenic in mice. Feeding CT to mice resulted not only in IgA antibody in intestinal secretions but also resulted in substantial plasma IgG and IgA antibody levels. Feeding KLH in much larger quantity resulted in little or no antibody response in intestinal secretions or plasma. Lymphoid cells from various tissues of mice fed CT were cultured in vitro for 10 days and the supernatant was tested for antibody to CT. Spontaneous antibody synthesis (no antigen added to cultures) was present in cultures of each cell type, but IgG anti-CT was found mainly in cultures of spleen and mesenteric lymph node cells and IgA anti-CT mainly in cultures of Peyer's patch and lamina propria cells. Peyer's patch cells cultured with CT as antigen synthesized both IgG and IgA anti-CT, suggesting that the antibody response to both isotypes originated in this site. Helper T cell activity for both IgA and IgG anti-CT was detected in spleens, mesenteric lymph nodes, and Peyer's patches. Lastly, when KLH and CT were fed to mice at the same time, an intestinal IgA anti-KLH and plasma IgG anti-KLH response was stimulated, a response pattern similar to that occurring to CT after CT was fed alone. We conclude that mucosal stimulation by CT generates both a systemic IgG and mucosal IgA response to this antigen, and that CT can cause a similar pattern of response to an unrelated protein antigen when both are administered into the intestine at the same time. The data favor the idea that both the IgG and IgA responses originate in GALT and then disseminate to other tissues. We propose that CT accomplishes these effects by altering the regulatory environment within GALT.

Administration, Oral↗
PubMed1984

Electrical activity of an intestinal epithelial cell line: hyperpolarizing responses to intestinal secretagogues.

Cultured epithelial cells (Intestine 407) derived from fetal human small intestine exhibited spontaneous oscillations of membrane potential between the resting level of about -20 mV and the activated level of about -75 mV. The cells were hyperpolarized to the latter level in response to mechanical or electrical stimuli. The hyperpolarizing responses were also elicited by the application of intestinal secretagogues: acetylcholine, histamine, serotonin and vasoactive intestinal polypeptide (VIP). The spontaneous oscillation of membrane potential became prominent and long-lasting in the presence of acetylcholine, histamine, serotonin or VIP. These secretagogue-induced responses were mediated by individual independent receptors on the cell membrane. Muscarinic receptors were responsible for the acetylcholine response, and H1-receptors for the histamine response. The cells also responded with a slow hyperpolarization to calcium ionophore A23187, which is known to induce intestinal secretion. The spontaneously occurring hyperpolarizing responses and those induced by stimuli were both due to an increase in the K+ conductance of the cell membrane. Since acetylcholine, histamine, serotonin and A23187 are known to promote mobilization of cellular Ca2+ ions in intestinal secretory cells, it is hypothesized that these electrical activities of the cell are closely related to the receptor stimulation which leads to the Ca2+-mediated intestinal secretion.

Acetylcholine↗
PubMed1977

Effect of indomethacin on cholera-induced fluid movement, unidirectional sodium fluxes, and intestinal cAMP.

Cholera enterotoxin (CT) produces intestinal secretion associated with an elevation of intestinal cyclic AMP (cAMP). Indomethacin, a potent inhibitor of prostaglandin (PG) synthesis, decreases CT-induced secretion, although a role for PG in this process has not been demonstrated. The purpose of this study was to measure the effects of indomethacin on net fluid movement and unidirectional Na fluxes in rabbit jejunal loops exposed to CT and to correlate these findings with intestinal cAMP levels. In untreated animals (no indomethacin), CT loops secreted 0.37 ml per cm per 4 hr compared to absorption in control loops of 0.23 ml per cm per 4 hr (P less than 0.001). In indomethacin-treated animals, there was a striking reduction of secretion in CT loops (0.07 ml per cm per 4 hr, P less than 0.001). Absorption in control loops in indomethacin animals was greater than in untreated animals (0.42 ml per cm per 4 hr, P less than 0.02). Unidirectional Na fluxes were greatly depressed in indomethacin animals at 1 h in both CT and control loops. This effect disappeared by 4 hr. Intestinal cAMP levels in CT loops, although not elevated at 1 hr despite the onset of secretion, were significantly elevated at 4 hr. Indomethacin did not alter cAMP levels at 1 and 4 hr in either cholera or control loops. These studies support the view that PG synthesis is not involved in CT-induced elevation of intestinal cAMP. Indomethacin may depress intestinal secretion by inhibiting a PG-mediated step beyond the generation of cAMP or by acting on some other, as yet unidentified, biological mechanism involved in intestinal secretion.

Animals↗