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PubMed1994

Nitric oxide involvement in sodium choleate-induced fluid secretion and diarrhoea in rats.

Bile salt-induced diarrhoea, net water and electrolyte secretion, gastrointestinal transit and nitric oxide (NO) synthase activity were studied in rats. NG-Nitro-L-arginine methyl ester (2.5-25 mg/kg i.p.), an inhibitor of NO synthase, and dexamethasone (0.03-0.3 mg/kg i.p.), an inhibitor of the inducible isoform of NO synthase, antagonized the diarrhoeal response. The NO precursor, L-arginine and isosorbide-5-mononitrate (an NO donor), reversed the inhibitory effect of NG-nitro-L-arginine methyl ester. The bile salt-stimulated fluid secretion, transit through the gut and NO synthase all were inhibited by NG-nitro-L-arginine methyl ester (but not NG-nitro-D-arginine methyl ester). NO synthase activity also was inhibited by dexamethasone. The results are consistent with bile salt induction of epithelial cell injury and concomitant synthesis of NO, mainly through activation of the inducible form of the enzyme. We believe that in this study NO is a mediator of intestinal secretion and motility changes that enhance transit of luminal contents through the gut, resulting in diarrhoea.

Amino Acid Oxidoreductases↗

PubMed1994

Cystic fibrosis heterozygote resistance to cholera toxin in the cystic fibrosis mouse model.

The effect of the number of cystic fibrosis (CF) alleles on cholera toxin (CT)-induced intestinal secretion was examined in the CF mouse model. CF mice that expressed no CF transmembrane conductance regulator (CFTR) protein did not secrete fluid in response to CT. Heterozygotes expressed 50 percent of the normal amount of CFTR protein in the intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion in intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion and fluid secretion suggests that CF heterozygotes might possess a selective advantage of resistance to cholera.

Alleles↗

PubMed1982

Immunological cross-reactivity of enterotoxins of Aeromonas hydrophila and cholera toxin.

Pre-incubation with anticholera toxin (ACT) significantly reduced intestinal secretion induced by cell-free broth preparations of heat-labile toxins (LT) of Escherichia coli and Aeromonas hydrophila in jejunal perfusion experiments in rats in vivo. Pre-incubation with ACT also prevented cytotoxicity by E. coli LT in the Y1 cell culture system. Pre-incubation had no effect on cytotoxicity in Y1 and L132 cell lines or on haemolytic activity with cell-free preparations of A. hydrophila. In another series of experiments rats were immunized with cholera toxin given as an intraperitoneal priming dose followed 12 days later by intraduodenal boosting. Immunization significantly protected against net intestinal fluid secretion induced by enterotoxigenic E. coli and A. hydrophila and by cholera toxin.

Aeromonas↗

PubMed1997

Kinetics of retinyl esters during postprandial lipemia in man: a compartmental model.

Orally ingested vitamin A (retinol) is incorporated into intestinal chylomicrons (CHYLO) in the form of retinyl esters (RE) along with newly absorbed dietary triglycerides (TG). As the intestinal lipoproteins undergo hydrolysis in the circulation, the majority of the RE remain with the secreted intestinal particles and have been used as a marker for intestinally derived lipoproteins during the early phase of the postprandial state. A multicompartmental model was developed for the kinetics of RE during postprandial lipemia in individuals with normal lipid levels (n = 16) and in patients with hyperlipidemia (n = 44). The assumptions used in the development of the model are presented in this report. Some of the key findings include (1) as much as 50% of the newly synthesized RE may be secreted by the intestine as very-low-density lipoprotein (VLDL)-sized particles of S(f) 20 to 400 following consumption of a test meal containing a moderate amount of fat (20 to 30 g); (2) in most individuals, approximately 50% of the RE secreted in S(f) greater than 400 are converted to smaller, less buoyant fractions, and 50% are irreversibly removed directly from the plasma; (3) as much as 5% to 20% of the ingested retinol may be secreted as small intestinal lipoproteins with the buoyance of low-density lipoprotein (LDL) in some individuals; and (4) less than 5% of RE flux through S(f) 20 to 400 is converted to S(f) less than 20, and the primary catabolic pathway for RE in this fraction is direct uptake. Comparable estimates can be obtained for the kinetic parameters when repeat studies are made in the same subjects under comparable conditions.

Apolipoproteins B↗

PubMed1991

Immunoadjuvant activity of oral Lactobacillus casei: influence of dose on the secretory immune response and protective capacity in intestinal infections.

Lactobacilli, often used as effectors of host functions, could play an important role in maintaining human health by controlling other intestinal microorganisms capable of producing harmful effects. Using an experimental model, we studied the effect of different oral doses of Lactobacillus casei on the secretory IgA response and the protective capacity of the microorganism in preventing intestinal infections. The optimization of the protective dose of Lb. casei by previous feeding and the use of the lactobacillus as an immunological way to control enteric infections were investigated. We found that conventional mice were protected against infection with Salmonella typhimurium and Escherichia coli by previous feeding for 2 consecutive days with a daily Lb. casei dose of 1.2 x 10(9) cfu/mouse. Previous feeding for 7 d proved less effective, and feeding for 5 d afforded no protection at all. We were also able to demonstrate that the protective effect of Lb. casei against Sal. typhimurium and Esch. coli was connected mainly with the high level of IgA antipathogen antibodies present in intestinal secretions. beta-Glucuronidase (EC 3.2.1.31) and beta-galactosidase (EC 3.2.1.23) activities, measured both in the intestinal fluid and histological samples, showed a marked increase in intestinal inflammatory response on day 5 of feeding. These results show that Lb. casei plays an important role in the prevention of enteric infections, a low dose being enough for protection against intestinal infections by increasing IgA secretion into the intestinal lumen, thus providing adequate defences for the mucosal surface. A previously administered dose of this magnitude could therefore be used as an oral adjuvant in preventing enteric infections.

Adjuvants, Immunologic↗

PubMed1984

Comparison of gastric and intestinal antisecretory and protective effects of prostacyclin and its stable thia-imino-analogue (Hoe 892) in conscious rats.

The effects of prostacyclin (PGI2) and its stable thia-thimo-analogue (Hoe 892) on gastric and intestinal secretions and gastric mucosal lesions have been determined in conscious rats. Both PGI2 and Hoe 892 given subcutaneously (s.c.) reduced dose-dependent gastric acid secretion, the ID50 (dose producing 50% inhibition) being about 48.6 and 11.8 micrograms/kg, respectively. In contrast, intragastric (i.g.) PGI2 and Hoe 892 did not cause any change in gastric acid secretion at doses ranging from 1 to 100 micrograms/kg. Both PGI2 and Hoe 892 reduced significantly intestinal fluid secretion (antienteropooling activity). PGI2 and Hoe 892 given i.g. or s.c. reduced dose-dependent gastric ulcer formation induced by acidified aspirin (ASA), Hoe 892 being somewhat less potent than PGI2. Both PGI2 and Hoe 892 were equally effective against gastric mucosal necrosis induced by absolute ethanol and this effect was observed both after i.g. and s.c. administration of these agents. We conclude that stable thia-imino-PGI2 analogue, Hoe 892, has similar gastric and intestinal antisecretory and protective activity as PGI2 and may be useful in the prevention of gastric damage by various noxious agents.

16,16-Dimethylprostaglandin E2↗

PubMed1982

Potentiating effect of bile on enterotoxin-induced diarrhea.

The influence of bile acids on adenosine 3',5'-phosphate-induced intestinal secretion was studied in mice. Bile flow was stopped by ligation of the common bile duct, and secretion was induced in ligated loops of the small intestine. The decrease of bile led to inhibition of hypersecretion after challenge with heat-labile enterotoxins from Vibrio cholerae and Escherichia coli, as well as with prostaglandin E1. In contrast, the fluid response induced by dibutyryl-adenosine 3',5'-phosphate was unaffected by intestinal bile. Injection of bile or bile acids into intestinal loops before cholera toxin challenge restored the toxin-induced secretion in the bile-depleted intestine. At the subcellular level the decrease of intestinal bile led to inhibition of cholera toxin-activated adenylate cyclase, whereas the bile concentration did not influence the binding of 125I-labeled toxin to the intestinal epithelial cells. The results suggest that intestinal bile interacts with adenylate cyclase in the induction of fluid secretion by enterotoxins and prostaglandin E1.

Adenylyl Cyclases↗

PubMed1995

Intestinal immune response induced in mice by staphylococcal enterotoxin B.

To investigate the induction of intestinal immunity to staphylococcal enterotoxins (SE) we have chosen the mouse as an experimental model. Since this species is devoid of emetic mechanism, SE can be administered orally without any loss. Mice were treated orally and/or parenterally with staphylococcal enterotoxin B (SEB). The anti-SEB response, either in serum or in the supernatant of in vitro cultured intestinal fragments was determined by enzyme immunoassay (EIA). The results showed that orally given SEB induced specific antibodies both in serum and intestinal secretions. Compared to oral route alone, parenteral followed by oral administration of SEB induced a higher intestinal response with IgA as predominant isotype. Although these results cannot directly be extrapolated to humans or animals with emetic reaction to SE, they do show the implication of intestinal immune system in response to this group of toxins.

Animals↗

PubMed1981

[14C]glucosamine incorporation into intestinal glycoproteins by calf intestinal epithelium in organ culture.

The uptake and incorporation of [14C]glucosamine into secreted intestinal glycoproteins was examined in the calf intestinal mucosa and isolated epithelial cells, using an organ culture system. Incorporation varied with the area of the intestine, ie duodenum greater than jejunum greater than ileum. Secreted glycoproteins were examined after 3 and 24 hours in organ culture. Initially, a glycoprotein approximately 68,000 molecular weight (mol wt) was secreted by all areas of the intestine. This was followed by the appearance of a larger glycoprotein 10(6) to 10(7) mol wt. Enzymatic cleavage of jejunal brush borders released a glycocalyx glycoprotein similar in size to the secreted large mol wt glycoprotein. These similarities in mol wt are only suggestive evidence that the 2 large glycoproteins are the same. This procedure allows for the study of the maturation and development of a poorly understood component of the intestinal epithelial cell which has a wide range of functional considerations.

Animals↗

PubMed1986

The effects of phorbol esters on fluid transport and blood flow in the small intestine.

Studies were designed to examine the effects of phorbol esters on intestinal fluid transport and blood flow in the anesthetized cat and enteropooling in the conscious rat. Intraluminal administration of phorbol ester into a segment of isolated small bowel produced a copious intestinal secretion and a concomitant mesenteric hyperemia in the cat. Net fluid movement in the intestine was converted from absorption in the control state to secretion following phorbol ester administration. Intravenous atropine reduced the phorbol ester-induced secretion by 56%; clonidine abolished the remaining secretory response. In the rat, intragastric administration of phorbol ester produced enteropooling comparable to that of other potent intestinal secretagogues. Since phorbol esters are known to activate protein kinase C, these studies suggest that activation of protein kinase C in the small intestine may lead to a full secretory response. The evidence suggests that this secretion is accompanied by a metabolic hyperemia. These results suggest that protein kinase C plays an important role in the regulation of intestinal fluid transport.

Animals↗

PubMed2000

Pathophysiological role of cholecystokinin in humans.

Cholecystokinin (CCK) is a major gastrointestinal hormone that plays an important role in stimulation of pancreatic secretion and gall-bladder contraction, regulation of gastrointestinal motility and induction of satiety. Ingestion of fat and protein induces significant increases in plasma CCK. Intraluminal mediators of CCK secretion, luminal CCK releasing factor and diazepam-binding inhibitor, were purified from rat intestinal secretion. These CCK-releasing factors (RF) are secreted tonically by the small intestine and stimulate CCK release. Another kind of CCK-RF named 'monitor peptide' was purified from the rat pancreatic juice that stimulates CCK secretion when introduced into rat intestine. Bile exclusion from the duodenum causes an increase in basal CCK and enhances stimulated plasma CCK release, and bile salt replacement reverses these effects. Thus, the CCK-RF are spontaneously secreted into the intestinal lumen in humans, while the CCK-producing cells are under constant suppression by intraduodenal bile acids. In acute pancreatitis, plasma CCK levels are high in patients with gallstone pancreatitis, but not in patients with pancreatitis from other causes, such as alcoholic and idiopathic pancreatitis. A transient disturbance of bile flow into the duodenum by stones or oedema of the pancreas together with impairment of pancreatic exocrine function might cause the increase in plasma CCK release in gallstone pancreatitis. Patients with chronic pancreatitis with mild to moderate impairment of exocrine function and abdominal pain, had significantly higher plasma CCK concentrations, whereas patients with pancreatic insufficiency had a significantly lower plasma CCK response to a test meal than the healthy subjects. The increased CCK may further aggravate pancreatitis and worsen the prognosis of pancreatitis by stimulating the injured pancreas, resulting in the vicious circle via endogenous CCK release. The CCK-A receptor antagonist might be therapeutically useful in acute pancreatitis by stopping the vicious circle.

Acute Disease↗

PubMed1981

The effect of bilirubin on the function of hamster small intestine.

Jaundice phototherapy is associated with a significant incidence of watery diarrhea. We have postulated that acute intestinal secretion, rather than malabsorption of dietary carbohydrate, is an effect of a photoproduct of bilirubin upon the intestinal mucosa. Because of major effect of phototherapy is the hepatic excretion of nonconjugated bilirubin, we investigated the effect of bilirubin on small intestinal function in the hamster in vivo. The entire small intestine was luminally perfused in vivo with solutions containing bilirubin (0.125 to 0.75 mmole/liter) and net water and sodium fluxes were measured. Control animals absorbed both water (J H2O(net) = 58.9 microliter/min/g) and sodium (J Na(net) = 4.55 microEq/min/g), but animals perfused with bilirubin (greater than or equal to 0.25 mmole/liter) exhibited secretion of water (J H2O(net) = -39.0--85.9) and sodium (J Na(net)=-9.91--18.24). The rate of water secretion was positively related to the concentration of bilirubin in the infusate (r=0.749; p less than 0.001). The concentration of bilirubin in ultrafiltrates of perfusate was likewise positively related to its concentration in the infusate (r = 0.844; p less than 0.001), indicating the potential importance of soluble forms of bilirubin in inducing secretion. Possible epithelial injury was studied by measuring the concentration of DNA in the perfusate and the activity of disaccharidases in postperfusion mucosa, and the possible role of cyclic adenosine monophosphate as a mediator of the secretory process was investigated by determining its concentration in postperfusion mucosa. Perfusion with 0.5 mM bilirubin, which produced significant secretion, did not cause loss of DNA (0.284 versus 0.244 mg/liter) or mucosal lactase activity (56 versus 53 units/g) or enhancement of cyclic adenosine monophosphate concentration (14.9 versus 14.12 pmoles/mg protein).

Animals↗

PubMed1978

Immune responses of sheep to the parasitic nematode Trichostrongylus colubriformis: infections in Thiry-Vella loops.

Some aspects of the local immune response to nematode infection were examined by introducing fourth-stage Trichostrongylus colubriformis larvae into Thiry-Vella loops in worm-free and T. colubriformis-resistant sheep. Approximately 15% of the larvae introduced into the worm-free sheep survived and matured into adult worms, whereas less than 1% survival in resistant sheep. The amount of IgG1, IgG2, IgM and albumin discharged from loops in worm-free but not resistant sheep all increased following infection with larvae. Secretions from resistant sheep contained approximately three times as much IgA as secretions from the worm-free group and, in addition, their plasma IgG1 level was significantly higher. Antibodies against T. columbriformis were found in both plasma and intestinal secretions, the highest titres being found in the resistant sheep. During worm expulsion from loops in the resistant sheep neither immunoglobulin levels nor antibody titres in the secretions increased significantly.

Animals↗

PubMed1999

IgA production in MHC class II-deficient mice is primarily a function of B-1a cells.

Mice deficient in MHC class II expression (C2d mice) do not make antibody to protein antigens administered systemically, but their ability to produce IgA antibody to antigen administered at mucosal sites has not been described. We investigated IgA production by C2d mice and their IgA antibody response to antigen given orally. Young C2d mice had normal amounts of serum IgA, intestinal-secreted IgA and normal numbers of intestinal IgA plasma cells, compared to control C57BL/6 mice. IgA production by C2d mice increased with age. Following oral immunization with cholera toxin, C57BL/6 mice responded with IgA and IgG antibody, and had increased numbers of IgA plasma cells, but C2d mice gave no response. The Peyer's patch and mesenteric lymph node tissues of C2d mice contained very few CD4-expressing T cells. Thus, C2d mice have no typical mucosal CD4 Th cells and cannot respond to a strong oral immunogen, yet they still produced and secreted IgA. We hypothesized that B-1 lymphocytes could provide a source of IgA independent of antigen-specific T cell help. Young C2d mice had normal numbers of peritoneal B-1a cells and their frequency increased with age. To test the role of these B-1a cells, we bred C2d mice to obtain mice that had no MHC class II expression and expressed the Xid gene that confers deficiency in B-1a cells. These double-deficient mice had 10-fold less serum and secreted IgA than all other F2 littermates. We conclude that B-1a cells are essential for the majority of IgA production in C2d mice. Thus, the C2d mouse may provide a useful tool for analysis of the role of intestinal IgA provided by B-1a cells.

Animals↗

PubMed1978

The influence of parathyroidectomy upon calcium and phosphate homeostasis in adult sheep.

The absorption and secretion of Ca and PO4 were measured with the use of radioactive isotopes in 4 adult sheep before and after parathyroidectomy. Secretion of Ca and PO4 into the stomach and intestines was measured separately. Parathyroidectomy resulted in a negative balance for Ca and PO4 and an accompanying fall in plasma Ca and PO4 concentrations. In the case of PO4 this response was attributed primarily to a reduced intestinal absorption, but for Ca increases in urinary excretion and intestinal secretion also contributed significantly. Secretion of PO4 to the stomach was reduced but endogenous PO4 excretion in the faeces was unchanged which indicated a reduced reabsorption of secreted PO4 by the intestines.

Animals↗

PubMed1992

Pharmacologic action of Escherichia coli heat-stable (STa) enterotoxin.

Escherichia coli produces a heat-stable (STa) enterotoxin that belongs to a family of peptides that mediate several diarrheal diseases, including traveler's diarrhea and epidemic diarrhea in infants and newborns. The STa enterotoxin consists of 18 or 19 amino acids and is encoded by genes specified on a transposon. Intestinal secretion is induced by specific binding to high affinity receptors that reside on the brush border cell membrane of the small intestine. Receptor activation by STa enterotoxin induces a sequence of events that culminate in the release of fluid and electrolytes into the intestinal lumen. These events include the stimulation of particulate guanylate cyclae and subsequent increase of intracellular cyclic GMP, involvement of particulate protein kinase, elevation of intracellular calcium, and activation of the phosphatidylinositol pathway. The release of archidonic acid and production of prostaglandins and/or leukotrienes have also been implicated in the action of STa. Evidence indicates that the STa enterotoxin receptor may be a single multifunctional membrane protein.

Amino Acid Sequence↗

PubMed1987

The effect of digoxin dosage on the digoxin-quinidine interaction in the bile duct-cannulated rat.

Pretreating anaesthetized bile duct-cannulated rats with 9 mg kg-1 quinidine significantly decreased the cumulative biliary excretion of digoxin and its metabolites after 10 or 100 micrograms kg-1 [3H]digoxin, although the effect was more marked in animals receiving the high dose of digoxin. In contrast, however, although quinidine pretreatment raised plasma radioactivity levels by 50-80% in animals given the higher dose of digoxin, no significant effect on circulating plasma levels was observed in rats receiving 10 micrograms kg-1 digoxin. Generally, quinidine had no statistically significant effect on other aspects of digoxin disposition, although with both digoxin doses there were trends towards a reduction in the direct intestinal secretion and urinary excretion of digoxin-derived radioactivity with an increase in tissue levels of radioactivity (apart from the small intestine wall where concentrations were reduced). The radioactivity in the bile after 100 or 10 micrograms kg-1 digoxin comprised about 25 and 33% of digoxin and digoxigenin bis-digitoxoside, respectively, as well as appreciable amounts of the monodigitoxoside and a highly polar component. This metabolite profile was unaffected by quinidine. The influence of cardiac glycoside dosage shown by the present work indicates that the digoxin-quinidine interaction and possibly analogous interactions involving other cardiac glycosides, may not always be readily detectable from plasma concentration data.

Animals↗

PubMed1989

Effect of jejunal infusion of nutrients on gastrointestinal transit and hormonal response in man.

The effects of jejunal infusion of nutrients on gastric emptying and secretion, intestinal transit and hormone release were studied in human volunteers. Two caloric loads, 1.3 and 3.3 kcal/min, of a nutrient solution consisting of 18 percent protein, 27 percent lipids, and 55 percent carbohydrates were tested. These were first used in random order in 6 subjects to assess the effects on intestinal transit. For the study of gastric emptying, jejunal infusion was started 1 h after intragastric instillation of a 490 kcal, 400 ml, homogenized meal. Intestinal transit time and gastric emptying half-time increased with the rate of nutrient infusion into the jejunum. Postprandial gastric secretion was reduced. The two caloric loads induced significant rises of plasma cholecystokinin and gastric inhibitory polypeptide concentrations. Plasma motilin decreased in relation to the jejunal caloric load. The other peptides were essentially not affected by jejunal nutrient infusion in fasting subjects. We conclude that in man, gastric emptying rate, gastric secretion, and intestinal transit are regulated by the presence of nutrients in the jejunum.

Adult↗