Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fluids and 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 685 records · Page 38Linked to original sources
PubMed1994

Effects of slaframine and 4-diphenylacetoxy-N-methylpiperidine methiodide (4DAMP) on pancreatic exocrine secretion in the bovine.

Three Holstein steers (345 +/- 22 kg) surgically fitted with a pancreatic cannula were used in two 3 x 3 Latin square design experiments to examine the effects of slaframine (SF), a muscarinic agonist, or 4-diphenylacetoxy-N-methylpiperidine methiodide (4DAMP), an M3 muscarinic glandular receptor antagonist, on pancreatic exocrine secretion. Pancreatic exocrine secretion was collected for 8 h postdosing at 30-min intervals beginning 1 h postfeeding. In experiment 1, steers were dosed with 0, 25, or 50 micrograms.kg-1 body weight (BW) of SF. Secretion of pancreatic juice and the pH of the secreted juice increased linearly (p < 0.05) with SF; however, secretion rate showed a time by treatment interaction (p < 0.05), as treatments converged 7 h postdosing. Trypsin secretion tended (p < 0.10) to show a quadratic response to SF administration, with the 25 micrograms SF.kg-1 BW dose having the lowest value. In experiment 2, steers received 50 micrograms.kg-1 BW of SF (positive control), 113 micrograms.kg-1 BW of 4DAMP (isosmolar with SF), or both. SF caused a greater pancreatic fluid secretion (p < 0.10) than 4DAMP, with SF plus 4DAMP intermediate. A time by treatment interaction (p < 0.04) was found, since treatments converged 8 h postdosing. Trypsin secretion was higher (p < 0.05) for SF than the other treatments. Chymotrypsin, alpha-amylase, and protein secretion were not affected. SF and 4DAMP alter pancreatic fluid secretion in the steer but have minimal effects on enzyme secretions.

Alkaloids↗
PubMed2000

The secreted effector protein of Salmonella dublin, SopA, is translocated into eukaryotic cells and influences the induction of enteritis.

Salmonella-induced enteritis is associated with the induction of an acute intestinal inflammatory response and net fluid secretion into the lumen of infected mucosa. Proteins secreted by the Inv/Spa type III secretion system of Salmonella play a key role in the induction of these responses. We have demonstrated recently that the Inv/Spa-secreted SopB and SopD effector proteins are translocated into eukaryotic cells via a Sip-dependent pathway and act in concert to mediate inflammation and fluid secretion in infected ileal mucosa. Mutations of both sopB and sopD significantly reduced, but did not abrogate, the enteropathogenic phenotype. This indicated that other virulence factors are involved in the induction of enteritis. In this work, we characterize SopA, a secreted protein belonging to the family of Sop effectors of Salmonella dublin. We demonstrate that SopA is translocated into eukaryotic cells and provide evidence suggesting that SopA has a role in the induction of enteritis.

Amino Acid Sequence↗
PubMed1991

Influence of age on antisecretory factor inhibition of enterotoxin action in the pig small intestine.

The effect of age on antisecretory factor (ASF) inhibition of cholera toxin (CT) and E. coli STa enterotoxin-induced fluid secretion in pig jejunum was investigated in vivo. Comparison was made between 2 week and 8 week old animals. ASF inhibited (P less than 0.05) CT-induced fluid secretion by up to 90% in the 8 week animals (from 18.4 +/- 5.87 mg/mg loop dry weight to 0.74 +/- 0.54 mg/mg loop dry weight). There was no effect of ASF on CT-secretion in the 14 day pigs suggesting that there is a minimum age before ASF is effective. ASF had no significant effect on net fluid transport after STa challenge in pigs from either age group. However, the predominant action of STa was to inhibit absorption and this would not be affected by ASF.

Aging↗
PubMed1980

Multiple effects of NA+ removal on pancreatic secretion in vitro.

The effects of removing Na+ from the incubation medium on basal and secretagogue induced zymogen release by pancreatic fragments and isolated pancreatic acini were studied by both morphological evaluation and measurement of amylase release. In both fragments and isolated acini, removal of Na+ led to an increased basal secretion of zymogen granule contents from acinar cells via exocytosis; secretory material, however, accumulated in acinar and ductular lumina as a result of the lack of fluid secretion necessary to wash out the enzymes. In studies with fragments, after Na+ removal there was no significant increase in amylase release into the medium; isolated acini, in contrast, showed an increased amylase release consistent with the shorter distance from the acinar lumen to the bathing medium. Stimulation with either bethanechol or caerulein led to a further delpletion of zymogen granules in both preparations; in the absence of Na+ secretory product accumulated in intracellular lakes as well as in duct lumens. The hypothesis that Na+ influx is important in stimulus-secretion coupling to release intracellular Ca2+ was directly tested by measuring 45Ca2+ efflux. No effect of removing Na+ on 45Ca2+ efflux was seen. It was concluded therefore, that while Na+ is essential for pancreatic fluid secretion, it is not necessary for the secretion of zymogen granule contents into acinar lumina.

Amylases↗
PubMed1985

The effects of morphine and enkephaline on gallbladder function in experimental cholecystitis. Inhibition of inflammatory gallbladder secretion.

Administration of morphine or its derivatives is the traditional way to treat biliary pain. Despite the common use of morphine and its analogues in patients with cholecystitis and biliary pain, their effects on the function of the inflamed gallbladder are not known. In the present study it is demonstrated that morphine usually contracts the normal gallbladder but does not influence the fluid transport across the mucosa. In experimental cholecystitis morphine and enkephaline do not further contract the gallbladder but, by specific opioid receptors, reduce the inflammatory fluid secretion by the mucosa. In case of obstruction of the gallbladder, fluid secretion by the mucosa will distend its wall and induce biliary pain. It is suggested that the pain-relieving effect of morphine in cholecystitis and attacks of biliary pain is mediated not only by a central analgesic effect but also by an influence on the function of the inflamed gallbladder.

Animals↗
PubMed1986

Blood flow distribution, lymph flow, villus tissue osmolality and fluid and electrolyte transport after exposing the cat small intestine to sodium deoxycholate.

The effect of luminal perfusion of a dihydroxy bile salt (sodium deoxycholate) on net fluid transport, intestinal haemodynamics, lymph flow, electrolyte transport and villus tissue osmolality was studied in cat jejunum. Furthermore, the effects of hexamethonium and tetrodotoxin, two drugs influencing nervous activity, were investigated. Concomitant to net fluid secretion, the bile salt increased mucosal blood flow whereas capillary filtration coefficient and lymph flow remained unchanged. Net sodium and chloride transport changed from absorption to secretion. The change of sodium transport was due to both an increased flux from tissue to lumen and a reduced flux in the opposite direction. Villus tissue hyperosmolality was reduced. None of the effects on intestinal haemodynamics correlated with the change in net fluid transport. Furthermore, hexamethonium and tetrodotoxin inhibited the secretion of fluid and electrolytes without influencing the induced changes in intestinal haemodynamics. It is concluded that the bile salt induces intestinal fluid secretion by stimulating an active secretory process in the crypts via enteric nerves. A minor part of the total change in net fluid transport may be due to a reduced uptake in the villi.

Animals↗
PubMed1982

Estrogen-mediated exocytosis in the glandular epithelium of prostates in castrated and hypophysectomized dogs.

Glandular cells in the prostate of the intact, adult dog contain numerous, large secretory granules that are released by exocytosis. Following hypophysectomy or castration, the glandular epithelium atrophies and the secretory granules degenerate and eventually disappear. Pharmacologic doses of estradiol-17 beta 17-cyclopentylpropionate cause the regressed glandular cells to synthesize a new population of smaller granules that are also released by exocytosis, even though estrogen is known to inhibit fluid secretion by the canine prostate. Thus, the mechanisms involved in prostatic synthesis and exocytosis of secretory granules are independent of those regulating fluid secretion and are operative in the absence of androgen or pituitary hormones.

Animals↗
PubMed2002

Role of various enterotoxins in Aeromonas hydrophila-induced gastroenteritis: generation of enterotoxin gene-deficient mutants and evaluation of their enterotoxic activity.

Three enterotoxins from the Aeromonas hydrophila diarrheal isolate SSU have been molecularly characterized in our laboratory. One of these enterotoxins is cytotoxic in nature, whereas the other two are cytotonic enterotoxins, one of them heat labile and the other heat stable. Earlier, by developing an isogenic mutant, we demonstrated the role of a cytotoxic enterotoxin in causing systemic infection in mice. In the present study, we evaluated the role of these three enterotoxins in evoking diarrhea in a murine model by developing various combinations of enterotoxin gene-deficient mutants by marker-exchange mutagenesis. A total of six isogenic mutants were prepared in a cytotoxic enterotoxin gene (act)-positive or -negative background strain of A. hydrophila. We developed two single knockouts with truncation in either the heat-labile (alt) or the heat-stable (ast) cytotonic enterotoxin gene; three double knockouts with truncations of genes encoding (i) alt and ast, (ii) act and alt, and (iii) act and ast genes; and a triple-knockout mutant with truncation in all three genes, act, alt, and ast. The identity of these isogenic mutants developed by double-crossover homologous recombination was confirmed by Southern blot analysis. Northern and Western blot analyses revealed that the expression of different enterotoxin genes in the mutants was correspondingly abrogated. We tested the biological activity of these mutants in a diet-restricted and antibiotic-treated mouse model with a ligated ileal loop assay. Our data indicated that all of these mutants had significantly reduced capacity to evoke fluid secretion compared to that of wild-type A. hydrophila; the triple-knockout mutant failed to induce any detectable level of fluid secretion. The biological activity of selected A. hydrophila mutants was restored after complementation. Taken together, we have established a role for three enterotoxins in A. hydrophila-induced gastroenteritis in a mouse model with the greatest contribution from the cytotoxic enterotoxin Act, followed by the Alt and Ast cytotonic enterotoxins.

Aeromonas hydrophila↗
PubMed1999

A novel plant-derived inhibitor of cAMP-mediated fluid and chloride secretion.

We have identified an agent (SP-303) that shows efficacy against in vivo cholera toxin-induced fluid secretion and in vitro cAMP-mediated Cl- secretion. Administration of cholera toxin to adult mice results in an increase in fluid accumulation (FA) in the small intestine (FA ratio = 0.63 vs. 1.86 in control vs. cholera toxin-treated animals, respectively). This elevation in FA induced by cholera toxin was significantly reduced (FA ratio = 0.70) in animals treated with a 100 mg/kg dose of SP-303 at the same time as the cholera treatment. Moreover, when SP-303 was administered 3 h after cholera toxin, a dose-dependent inhibition of FA levels was observed with a half-maximal inhibitory dose of 10 mg/kg. In Ussing chamber studies of Caco-2 or T84 monolayer preparations, SP-303 had a significant effect on both basal current and forskolin-stimulated Cl- current. SP-303 also induced an increase in resistance that paralleled the observed decrease in current. These data suggest that SP-303 has an inhibitory effect on cAMP-mediated Cl- and fluid secretion. Thus SP-303 may prove to be a useful broad-spectrum antidiarrheal agent.

Animals↗
PubMed1998

Experimental study of antidiarrheal activity of Salicairine.

Experimental antidiarrheal activity of a traditionally used medication, Salicairine, was demonstrated in comparison to loperamide by significant inhibition of castor oil-induced diarrhea in mice (increases in hard faeces/total faeces ratio of 38 and 54 and 5 and 54% with respect to controls, at 0.5 and 1 mL/kg and 1 and 2 mg/kg, respectively) and bisacodyl-induced increase in large intestine transit in rats (125 and 280 and 210% with respect to controls, at 0.4 and 2 mL/kg Salicairine and 5 mg/kg loperamide, respectively). Salicairine was able to reduce contractions of isolated rat duodenum induced by barium chloride and acetylcholine, although not completely (that is about 60%) as seen with loperamide. Also, it did not change normal gastrointestinal transit in mice at doses of 0.5 to 1 mL/kg, conversely to loperamide which had a significant effect (decrease of 50%) at 2 mg/kg. Finally, Salicairine at 0.01 mL/mL, like loperamide at 0.2 mg/mL, significantly increased net fluid absorption in rat colon, either in basal conditions (30 and 64% respectively) or after a prostaglandin E1-induced increase in net fluid secretion (41 and 35%, respectively). The antidiarrheal activity of Salicairine is possibly related, at least in part, to an increase in colon net fluid absorption or a decrease in net fluid secretion.

Acetylcholine↗
PubMed1998

Antisera to selected outer membrane proteins of Vibrio cholerae protect against challenge with homologous and heterologous strains of V. cholerae.

Each year cholera epidemics occur in various places around the world. Though there is no effective vaccine against cholera, people who recover from an infection usually have prolonged immunity to the disease. Sera from convalescent patients contain antibodies to a number of outer membrane proteins (OMPs) of V. cholerae. We isolated several OMPs (43, 42, 30, and 22 kDa) from V. cholerae V86 E1 Tor Inaba, sequenced their amino-termini, and generated hyperimmune sera against them in rabbits. Antisera to the 43-, 42-, and 22-kDa OMPs, but not the preimmune sera, significantly reduced V. cholerae-induced fluid secretion seen in rabbit intestinal loops challenged with the homologous strain. In addition, a combination of antisera to the different OMPs reduced the fluid secretion induced by challenge with heterologous V. cholerae Ogawa and O139 strains. These results have significance in the development of vaccines to V. cholerae, as the hyperexpression of these OMP encoding genes in vaccine strains may improve the efficacy of cholera vaccines.

Adhesins, Bacterial↗
PubMed1978

Species differences in contractility of seminiferous tubules and tunica albuginea as related to sperm transport through the testis.

Frequency and depth of contractions and tonus--i.e., diameter of the tubule or shift of the baseline for the capsule--of both the seminiferous tubules and the tunica albuginea were quantified for rat, mouse, rabbit, hamster and ground squirrel tests. In the ground squirrel, contractility was measured prior to, during and after breeding. The rat testes had the strongest tubular contractions; those of the mouse, squirrel and rabbit exhibited intermediate values, and the hamster tests had the weakest tubular contractions. The rabbit tests exhibited the strongest, most well-developed rhythmical capsular contractions while the rat, mouse, hamster and squirrel tests showed no definite rhythmical contractions. Hamster tests apparently depend primarily upon fluid secretion by the seminiferous tubules for sperm transport through the tests to the epididymis, while the squirrel, rat and mouse tests utilize both fluid secretion and some tubular contractions. The rat apparently utilizes tubular contractions more so than the other rodents studied for sperm transport.

Animals↗
PubMed1981

Indomethacin intravenously--a new way for effective relief of biliary pain: a double-blind study in man.

Prostaglandins have been demonstrated to contract the gallbladder and induce fluid secretion into its lumen in experimental animals. Indomethacin is an effective inhibitor of prostaglandin synthetase and has recently been demonstrated to inhibit inflammatory fluid secretion into the gallbladder in experimental cholecystitis. A mechanism by which an increased prostaglandin synthesis will result in a raised intraluminal pressure in the gallbladder in patients with gallstone disease has been suggested. By inhibiting the synthesis of prostaglandins with indomethacin the intraluminal pressure is reduced and the biliary pain relieved. In a double-blind study with a placebo in 40 separate attacks of biliary pain in 37 patients with verified gallstone disease intravenous indomethacin was found to effectively relieve pain within 5 to 30 minutes. No serious side effects were seen, but nausea and vertigo of short duration were noticed in 10 of 21 cases of indomethacin treatment. The drug did not affect blood pressure, but a reduction of the pulse rate was usually seen.

Adult↗
PubMed1993

Tumor necrosis factor-alpha mediates the early pathology in Salmonella infection of the gastrointestinal tract.

Salmonella infection of the intestinal tract results in damage to the gut epithelium. While it is generally believed that bacteria and/or bacterial products account for this pathology, the role of host factors has not been explored. Using a ligated intestinal loop model, we investigated whether tumor necrosis factor-alpha (TNF-alpha) could contribute to the tissue pathology associated with Salmonella infection. Intestinal segments infected with Salmonella typhimurium had high levels of fluid secretion as early as 6 h post-bacterial infection. At this time point, low levels of TNF activity were also present in the fluid obtained from infected segments. At 20 h post-infection, high levels of TNF activity were present in fluids obtained from infected intestinal segments and was characterized as TNF-alpha by neutralization experiments using rabbit antisera to TNF-alpha. TNF-alpha production was further verified by Northern blot analysis using RNA obtained from cells eluted from the infected intestinal segments. In contrast, no TNF activity was found in fluid obtained from intestinal segments challenged with cholera toxin, which induces fluid secretion with little to no inflammatory response. Double labeling by in situ hybridization and immunocytochemistry revealed that macrophages in the lamina propria were producing the TNF-alpha mRNA. To investigate what role TNF-alpha might play in Salmonella-induced inflammation, intestinal segments were injected with recombinant mouse TNF-alpha (rTNF-alpha) or mice were pretreated with antibody to TNF-alpha or a control antibody prior to Salmonella infection. The histological profile of intestinal segments injected with rTNF-alpha appeared identical to segments infected with S. typhimurium. Further, pathology was completely eliminated in infected mice pretreated with antibody to TNF-alpha. These results document the production of TNF-alpha in the intestinal tract following S. typhimurium infection and show that the early pathology induced by Salmonella infection of the gastrointestinal tract is mediated by immune mechanisms.

Animals↗
PubMed2006

Hyposecretion, not hyperabsorption, is the basic defect of cystic fibrosis airway glands.

Human airways and glands express the anion channel cystic fibrosis transmembrane conductance regulator, CFTR, and the epithelial Na(+) channel, ENaC. Cystic fibrosis (CF) airway glands fail to secrete mucus in response to vasoactive intestinal peptide or forskolin; the failure was attributed to loss of CFTR-mediated anion and fluid secretion. Alternatively, CF glands might secrete acinar fluid via CFTR-independent pathways, but the exit of mucus from the glands could be blocked by hyperabsorption of fluid in the gland ducts. This could occur because CFTR loss can disinhibit ENaC, and ENaC activity can drive absorption. To test these two hypotheses, we measured single gland mucus secretion optically and applied ENaC inhibitors to determine whether they augmented secretion. Human CF glands were pretreated with benzamil and then stimulated with forskolin in the continued presence of benzamil. Benzamil did not rescue the lack of secretion to forskolin (50 glands, 6 CF subjects) nor did it increase the rate of cholinergically mediated mucus secretion from CF glands. Finally, neither benzamil nor amiloride increased forskolin-stimulated mucus secretion from porcine submucosal glands (75 glands, 7 pigs). One possible explanation for these results is that ENaC within the gland ducts was not active in our experiments. Consistent with that possibility, we discovered that human airway glands express Kunitz-type and non-Kunitz serine protease inhibitors, which might prevent proteolytic activation of ENaC. Our results suggest that CF glands do not display excessive, ENaC-mediated fluid absorption, leaving defective, anion-mediated fluid secretion as the most likely mechanism for defective mucus secretion from CF glands.

Amiloride↗
PubMed2001

The peptide YY-preferring receptor mediating inhibition of small intestinal secretion is a peripheral Y(2) receptor: pharmacological evidence and molecular cloning.

A peptide YY (PYY)-preferring receptor [PYY > neuropeptide Y (NPY)] was previously characterized in rat small intestinal crypt cells, where it mediates inhibition of fluid secretion. Here, we investigated the possible status of this receptor as a peripheral Y(2) receptor in rats. Typical Y(2) agonists (PYY(3-36), NPY(3-36), NPY(13-36), C2-NPY) and very short PYY analogs (N-alpha-Ac-PYY(22-36) and N-alpha-Ac-PYY(25-36)) acting at the intestinal PYY receptor were tested for their ability to inhibit the binding of (125)I-PYY to membranes of rat intestinal crypt cells and of CHO cells stably transfected with the rat hippocampal Y(2) receptor cDNA. Similar PYY preference was observed and all analogs exhibited comparable high affinity in both binding assays. The same held true for the specific Y(2) antagonist BIIE0246 with a K(i) value of 6.5 and 9.0 nM, respectively. BIIE0246 completely abolished the inhibition of cAMP production by PYY in crypt cells and transfected CHO cells. Moreover, the antagonist 1) considerably reversed the PYY-induced reduction of short-circuit current in rat jejunum mucosa in Ussing chamber and 2) completely abolished the antisecretory action of PYY on vasoactive intestinal peptide (VIP)-induced fluid secretion in rat jejunum in vivo. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) experiments showed that Y(2) receptor transcripts were present in intestinal crypt cells (3 x 10(2) molecules/100 ng RNA(T)) with no expression in villus cells, in complete agreement with the exclusive binding of PYY in crypt cells. Finally, a full-length Y(2) receptor was cloned by RT-PCR from rat intestinal crypt cells and also from human small intestine. We conclude that the so-called PYY-preferring receptor mediating inhibition of intestinal secretion is a peripheral Y(2) receptor.

Amino Acid Sequence↗
PubMed1979

Diffusion-like process can account for protein secretion by the pancreas.

When fluid secretion by the pancreas was mechanically blocked, amylase secretion into the duct ceased. When flow was reduced in a graded fashion by the application of a back pressure, amylase output was reduced proportionately and amylase concentration in secretion was maintained constant. Thus, the secretion of digestive enzyme from the cell into the duct appears to be dependent upon the concentration of enzyme in the duct system. This behavior is most simply explained by diffusion-like (concentration dependent, bidirectional) fluxes of digestive enzyme across the plasma membrane. A unidirectional process, such as exocytosis, whose rate should be unaffected by fluid flow, cannot readily explain these results.

Amylases↗
PubMed1984

Studies with enterotoxigenic microorganisms: effects of candidate antidiarrhoeals in experimental animals in vivo.

Chlorpromazine or aspirin alone, when given to rats parenterally, reduced intestinal fluid secretion induced by cell-free preparations of enterotoxigenic organisms including Escherichia coli, Aeromonas hydrophila, Staphylococcus pyogenes, and Salmonella typhimurium. A combination of chlorpromazine-aspirin given parenterally caused much more marked reduction of fluid secretion. Indomethacin also had significant antisecretory effects against a range of bacterial enterotoxins, while loperamide was effective against heat-labile toxin (LT)-positive E. coli and A. hydrophila. Nicotinamide increased net fluid absorption in the presence of E. coli LT, A. hydrophila, and S. typhimurium. Of the adsorbents tested, aluminum hydroxide showed a positive effect only with E. coli LT and A. hydrophila, while cholestyramine affected net fluid flux only with E. coli ST (heat-stable toxin). Charcoal was effective against all microorganisms tested but only when premixed with the perfusate before the experiments. Aspirin and chlorpromazine probably act at multiple sites to decrease intestinal secretion, and the combination of low doses of these drugs with possibly different sites of action may have advantages over a single agent used in high dosage.

Aluminum Hydroxide↗