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At least 847 records · Page 47Linked to original sources
PubMed1994

Management of the short bowel syndrome.

The short bowel syndrome has become an increasingly common clinical condition. Malnutrition and its complications should be avoidable with use of a combination of enteral and parenteral nutrition support. Dietary management needs to be individualized. Drugs directed against gastric hypersecretion, increased motility, intestinal secretion, unabsorbed bile salts, and bacterial overgrowth improve intestinal function. Complications specific to the short bowel syndrome (gastric hypersecretion, cholelithiasis, nephrolithiasis) can be minimized and diagnosed early. Surgical management includes preserving intestinal remnant length and improving its function. Intestinal transplantation is evolving as a promising therapeutic alternative for patients with complications of long-term parenteral nutrition support.

Humans↗
PubMed1999

Interruption of transmembrane signaling as a novel antisecretory strategy to treat enterotoxigenic diarrhea.

Bacteria that produce heat-stable enterotoxins (STs), a leading cause of secretory diarrhea, are a major cause of morbidity and mortality worldwide. ST stimulates guanylyl cyclase C (GCC) and accumulation of intracellular cyclic GMP ([cGMP]i), which opens the cystic fibrosis transmembrane conductance regulator (CFTR)-related chloride channel, triggering intestinal secretion. Although the signaling cascade mediating ST-induced diarrhea is well characterized, antisecretory therapy targeting this pathway has not been developed. 2-ChloroATP (2ClATP) and its cell-permeant precursor, 2-chloroadenosine (2ClAdo), disrupt ST-dependent signaling in intestinal cells. However, whether the ability to disrupt guanylyl cyclase signaling translates into effective antisecretory therapy remains untested. In this study, the efficacy of 2ClAdo to prevent ST-induced water secretion by human intestinal cells was examined. In Caco-2 human intestinal cells, ST increased [cGMP]i, induced a chloride current, and stimulated net basolateral-to-apical water secretion. This effect on chloride current and water secretion was mimicked by the cell-permeant analog of cGMP, 8-bromo-cGMP. Treatment of Caco-2 cells with 2ClAdo prevented ST-induced increases in [cGMP]i, chloride current and water secretion. Inhibition of the downstream consequences of ST-GCC interaction reflects proximal disruption of cGMP production because 8-bromo-cGMP stimulated chloride current and water secretion in 2ClAdo-treated cells. Thus, this study demonstrates that disruption of guanylyl cyclase signaling is an effective strategy for antisecretory therapy and provides the basis for developing mechanism-based treatments for enterotoxigenic diarrhea.

2-Chloroadenosine↗
PubMed1990

Interleukins 1 and 3 stimulate anion secretion in chicken intestine.

Interleukin 1 or 3 added to the serosal side of chicken small intestine transiently increases short-circuit current. Replacement of bathing-medium Cl and HCO3 with gluconate and HEPES abolished the short-circuit current increase, consistent with these cytokines stimulating electrogenic anion secretion. Cytokine-stimulated short-circuit current changes were inhibited by preincubation with piroxicam (10(-5) M), an inhibitor of arachidonic acid cyclooxygenase, suggesting prostaglandin formation as an intermediate step for cytokine stimulation of short-circuit current. In intact mucosal strips, interleukin 1 and 3 stimulated prostaglandin E2 release and elevated tissue 3',5'-cyclic adenosine monophosphate concentration. When prostaglandin E2 release from epithelial and subepithelial fractions of the mucosa by interleukin 1 was determined, increases were found only from the subepithelium. The secretory actions of cytokines appear to be mediated by arachidonic acid metabolites most likely produced by cells of the lamina propria and submucosa and may play a role in inflammatory processes in which intestinal secretion is enhanced.

Action Potentials↗
PubMed1993

Inhibition of intestinal motility and secretion by flavonoids in mice and rats: structure-activity relationships.

Intraperitoneal administration of some flavonoids (apigenin, flavone, kaempferol, morin, myricetin, naringin and rutin; 12.5-50 mg kg-1) significantly (P < 0.05-0.01) reduced small (28-69%) and large (83-134%) intestinal transit in mice. Other flavonoids (naringenin, silibinin, silymarin and taxifolin, 100-200 mg kg-1) reduced (23-41%; P < 0.05-0.01) intestinal transit at doses of 100-200 mg kg-1 while hesperitin, catechin and phloridzin (up to 200 mg kg-1) had no effect. This effect was antagonized by yohimbine (87-96%) and phentolamine (87-91%) but not by prazosin, propranolol, atropine, hexamethonium, mepyramine, cyproheptadine and naloxone. Yohimbine (92-96%) also antagonized the inhibitory effect of flavonols (12.5-50 mg kg-1) (P < 0.05-0.01) on intraluminal accumulation of fluid and diarrhoea induced by castor oil. By contrast, verapamil potentiated the flavonol effect. It is suggested that these effects, influenced by the structure of the molecules, are mediated by alpha 2-adrenergic receptors and calcium.

Animals↗
PubMed1998

Drug exsorption from blood into the gastrointestinal tract.

Drugs are exsorbed from the blood across the gastrointestinal membranes by passive or active processes. In the case of a passive transport mechanism, the exsorption of drugs depends on the concentration gradients between the serosal and mucosal sides. The extent of secretion (exsorption) is determined by numerous factors such as extent of binding to serum proteins, distribution volume, lipophilicity, pKa and molecular size of drugs, and the blood flow rate in the gut. Specific transport systems such as P-glycoprotein (P-gp), organic cation and organic anion transporters are found to be involved in active intestinal secretion of drugs. Intestinal secretory transport systems reduce the extent of drug absorption sometimes resulting in low oral bioavailability. It is, therefore, important to know whether poor drug absorption is due to the involvement of specialized secretory transport systems. Modulation of intestinal secretory transport can be a means to enhance absorption of drugs with low oral bioavailability if exsorption of drugs is based on active secretion pathways that are open for control from the "outside".

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1975

[Interrelationship of the cardiovascular and digestive systems in the genesis of experimental atherosclerosis].

In chronic experiments (up to 2 years) on dogs on atherogenic diets the motor activity of the gastrointestinal tract, cholesterol, the phospholipid level in the blood and in the intestinal secretion as well as the morphology of the small intestine and the vascular system were examined. At the early stages of atherosclerosis (up to 4 months) the rise of the blood cholesterol level was followed by an increase in the periods of the activity of the gastrointestinal tract, a rise of cholesterol discharge by the small intestine, and the development of the hypertrophic process in the mucous membrane. At the later stages a change in the mucous membrane of the small intestine was observed with development of a dystrophic-atrophic process, a disturbance of motor activity of the gastrointestinal tract and of the correlations between the cholesterol content in the blood and its discharge by the small intestine. This period was characterized by a high and persistent hypercholesterolemia and pronounced atherosclerotic changes in the vascular system.

Adaptation, Physiological↗
PubMed1981

Jejunal water and electrolyte secretion induced by L-arginine in man.

In this study a perfusion technique has been used to investigate jejunal secretion in response to the dibasic amino acid L-arginine. L-arginine at 5, 15, and 40 mmol/l in isotonic saline solutions induced net intestinal secretion of water and Na+. The structurally similar dibasic amino acid L-lysine caused net absorption at 5 and 15 mmol/l, and only modest net secretion of water and Na+ at 40 mmol/l, although absorption rates of the two amino acids were similar. D-arginine (15 mmol/l) was without effect on net water and Na+ absorption. L-arginine 15 mmol/l inhibited glucose-stimulated water and Na+ absorption when perfused in the same intestinal segment, but was without effect when perfused in separate jejunal or ileal segments. Parenteral chlorpromazine inhibited L-arginine induced jejunal water and Na+ secretion. Jejunal secretion induced by L-arginine thus appears not to be due to passive osmotic water flow, nor to release of circulating secretagogues. Stimulation of a mucosal secretory process is most likely to be the mechanism.

Adult↗
PubMed1984

Colonic secretion mediated by prostaglandin E2 and 5-hydroxytryptamine may contribute to diarrhea due to morphine withdrawal in the rat.

Prostaglandins and cyclic adenosine monophosphate have been claimed to play a major role in the morphine withdrawal syndrome, but intestinal secretion has not been ruled out as being responsible, at least in part, for the accompanying diarrhea. Therefore, experiments were performed in which the effect of naloxone-induced morphine withdrawal on jejunal and on colonic fluid transport was assessed in tied-off loops of rat intestine in vivo simultaneously with mucosal cyclic adenosine monophosphate levels or colonic luminal release of prostaglandin E2 or 5-hydroxytryptamine. Naloxone-induced withdrawal reversed fluid absorption to secretion without changing cyclic adenosine monophosphate levels, but markedly enhanced local prostaglandin E2 and 5-hydroxytryptamine release (p less than 0.01). Indomethacin and the 5-hydroxytryptamine receptor antagonist ketanserin prevented withdrawal-induced fluid secretion and the increase in prostaglandin E2 release without influencing the release of 5-hydroxytryptamine. In addition, the alpha 2-adrenergic receptor agonist clonidine promoted absorption during withdrawal, whereas atropine failed to influence fluid transport. These data suggest that naloxone-precipitated intestinal fluid secretion may contribute to diarrhea due to morphine withdrawal and that 5-hydroxytryptamine may play an important role in mediating this secretion through stimulation of local prostaglandin formation.

Animals↗
PubMed1980

[Lysozyme in the material and the digestive secretions of the domestic rabbit].

Lysozyme is present in the salivary secretions and a low level has been reported for the bile and the pancreatic juice. It has been found to be absent from the digestive material of the rabbit stomach and small and large intestines as well as from the intestinal secretions taken from temporary fistulae placed at the duodenal, jejunal, ileal and colic levels. However, secretions obtained by permanent intestinal and gastric fistulae showed high enzyme levels. Lysozyme is thus of probable plasmatic origin. The question of Paneth cell secretion is still to be determined.

Animals↗
PubMed2005

Diversity in secreted PLA2-IIA activity among inbred mouse strains that are resistant or susceptible to Apc Min/+ tumorigenesis.

The secreted phospholipase A2 type IIA (Pla2g2a) gene was previously identified as a modifier of intestinal adenoma multiplicity in Apc Min/+ mice. To determine if intestinal secreted phospholipase A2 (sPLA2) activity was also attenuated in susceptible strains, we developed a sensitive assay to directly quantitate sPLA2 activity in the murine intestinal tract utilizing a fluorescent BODIPY-labeled phospholipid substrate. Here, we report assay conditions that distinguish between secreted and cytosolic PLA2 enzyme activities in extracts of intestinal tissue. The small intestine exhibited higher activity levels than the large intestine. Consistent with predictions from the sPLA2-IIA gene sequence in inbred strains, we detected low levels of enzyme activity in inbred strains containing sPLA2-IIA mutations; these strains were also associated with greater numbers of intestinal polyps. Additionally, the assay was able to distinguish differences in levels of sPLA2 activity between neoplasia-resistant strains, which were then shown by sequencing to carry variant wild-type sPLA2-IIA alleles. Immunohistochemical analyses of intestinal tissues were consistent with sPLA2-IIA activity levels. This approach enables further studies of the mechanisms of sPLA2 action influencing the development and tumorigenesis of the small intestine and colon in both mice and humans.

Amino Acid Sequence↗
PubMed1981

Ricinoleic acid causes secretion in autotransplanted (extrinsically denervated) canine jejunum.

To examine the role of extrinsic nerves and hormones in intestinal secretion of fluid, we studied the effect of ricinoleic acid on absorption by isolated, autotransplanted jejunal loops in four dogs. Compared to perfusion with control solution, the addition of ricinoleic acid caused reversible secretion of water and electrolytes and inhibition of glucose absorption, as previously described in the innervated intestine. In contrast, oral castor oil caused diarrhea but had no effect on absorption from the denervated loop. Thus, the secretory action of ricinoleic acid is maintained without the influence of extrinsic nerves; in addition, further support is added to the proposal that hormones do not mediate secretion in this model. These findings support a local mechanism for the secretion induced by ricinoleic acid.

Animals↗
PubMed2002

Inhibitory effects of octreotide on luminal cholecystokinin-releasing factor, plasma cholecystokinin, and pancreatic secretion in conscious rats.

INTRODUCTION: Luminal cholecystokinin-releasing factor (LCRF), purified from rat intestinal secretions, is an intraluminal regulator of cholecystokinin (CCK) secretion during bile and pancreatic juice diversion. AIM: Because the LCRF content was not influenced by intravenous administration of atropine or somatostatin, the inhibitory effect of a potent somatostatin analog octreotide on LCRF content, the plasma CCK level, and pancreatic secretion was examined. METHODOLOGY: Rats were prepared with bile and pancreatic cannulae and two duodenal cannulae and with an external jugular vein cannula. After 1.5-hour basal collection, bile and pancreatic juice was diverted for 2 hours, during which octreotide was infused intravenously or into the duodenal lumen. The changes in pancreatic secretion were recorded for 2 hours, and the plasma CCK level and LCRF content 2 hours after the treatment were measured. RESULTS: Bile and pancreatic juice diversion significantly increased pancreatic secretion and plasma CCK and LCRF levels. Intravenous infusion of octreotide (0.2 and 0.5 nmol/kg/hour) inhibited all parameters. Intraduodenal infusion of a lower dose of octreotide (33 nmol/kg/hour) inhibited pancreatic secretion, but did not inhibit CCK release or LCRF content. The higher doses (100 and 300 nmol/kg/hour) inhibited all parameters. CONCLUSION: Intravenous and intraduodenal administrations of octreotide inhibited CCK release and LCRF content and pancreatic secretion induced by bile and pancreatic juice diversion.

Animals↗
PubMed1997

Guanylin-, heat-stable enterotoxin of Escherichia coli- and vasoactive intestinal peptide-induced water and ion secretion in the rat intestine in vivo.

The heat-stable enterotoxin of Escherichia coli binds to an intestinal receptor, guanylyl cyclase-C, and produces cGMP to induce diarrhea. Guanylin is an endogenous ligand of this receptor. In the present in vivo study, the intestinal water and ion secretion induced by mucosal application of 2 nmol/ml guanylin or 5 or 10 units/ml heat-stable enterotoxin into closed loops was compared in the rat. The characteristics of secretion induced by cAMP following intravenous perfusion of 1.2 nmol/100 g per h vasoactive intestinal peptide were compared to those induced by cGMP. Unidirectional Na+ and Cl- fluxes were estimated by addition of 22Na into the loop and i.v. injection of 36Cl. Guanylin induced less water and ion secretion than that produced by heat-stable enterotoxin in the colon, confirming the results of in vitro studies, and also in duodenum and ileum. The cAMP- or cGMP-mediated response had a similar pattern, i.e., an inhibition of Na+ absorption and an increase in anion secretion.

Animals↗
PubMed1994

HCO3- secretion by rat distal colon: effects of inhibitors and extracellular Na+.

BACKGROUND/AIMS: The large intestine secretes HCO3- via a Cl-/HCO3- exchange mechanism located in the apical membrane of colonocytes. However, an additional transport system(s) must facilitate HCO3- (OH-) entry or H+ exit across the basolateral cell surface. The aim of this study was to determine that mechanism(s). METHODS: A modified Ussing apparatus was used to measure net HCO3- secretion in segments of rat distal colon. RESULTS: When added to the serosal solution, 10 mmol/L 4-acetamido-4'-isothiocyano-2,2'-disulfonic acid stilbene (SITS), 1 mmol/L SITS and 0.1 mmol/L diisothiocyanostilbene-2,2'-disulfonic acid, inhibited HCO3- secretion by 88%, 51%, and 30%, respectively. However, the Na+/H+ exchange inhibitors, amiloride (1 mmol/L), dimethylamiloride (0.1 mmol/L), ethylisopropylamiloride (0.1 mmol/L), failed to affect HCO3- secretion. Acetazolamide (1 mmol/L) blocked HCO3- secretion by approximately 60% when in the serosal solution but had little effect when in the mucosal solution. Ion substitution studies showed that HCO3- secretion required Na+ in the serosal solution (K0.5 approximately 12 mmol/L). HCO3- secretion was unaffected by depolarizing the basolateral membrane potential with K(+)-rich medium. CONCLUSIONS: These data are consistent with Na+ linked HCO3- transport across the colonocyte basolateral membrane, which appears to be electroneutral.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1993

Oral prostaglandin E2 prevents gut atrophy during intravenous feeding but not bacterial translocation.

The pathophysiologic changes in gut physiology that result in bacterial translocation during intravenous feeding are poorly defined, though believed to be related in part to intestinal atrophy, decreased mesenteric blood flow, and lack of intestinal secretions. This study investigated the hypothesis that pharmacologic preservation of intestinal structure and function by orally administered 16,16-dimethyl-prostaglandin E2 would prevent bacterial translocation in intravenously fed rats. Thirty-five rats were randomized to three groups: group 1 was fed rat chow ad libitum, group 2 received standard parenteral nutrition, and group 3 received parenteral nutrition plus oral 16,16-dimethyl-prostaglandin E2 (150 micrograms/kg twice a day). Rats were fed there respective diets for 5 days and killed. Mesenteric lymph nodes were procured for culture, and the intestine was assessed for weight, DNA, protein values, and histologic character. Results demonstrate that orally administered 16,16-dimethyl-prostaglandin E2 potently attenuates the intestinal atrophy associated with parenteral feeding but does not prevent bacterial translocation. Intestinal barrier dysfunction and bacterial translocation during intravenous feeding is related to factors other than the development of gut atrophy.

Administration, Oral↗