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1.
Am J Physiol Regul Integr Comp Physiol ; 278(6): R1589-94, 2000 Jun.
Article in English | MEDLINE | ID: mdl-10848528

ABSTRACT

This study examined the effect of fasting on the neural control of ion transport and paracellular permeability in piglet jejunum. Muscle-stripped tissues from fed or 48-h fasted piglets were mounted in Ussing chambers. Neural blockade with tetrodotoxin (TTX) or antagonists of muscarinic or nicotinic receptors caused reductions in basal short-circuit current that were approximately threefold greater in fasted piglets. The TTX-induced reduction in short-circuit current in fasted piglets was due to a decrease in residual ion flux and was abolished in the absence of HCO(-)(3). Intestinal paracellular permeability, as indicated by tissue conductance (G(t)) and fluxes of inulin and mannitol, was significantly increased by fasting. TTX increased inulin flux and G(t) in fed but not fasted piglets. In fasted piglets, carbachol reduced G(t) by 29% and mannitol flux by 27% but had no effect on these parameters in the fed state. We conclude that fasting enhances enteric neural control of basal ion transport and increases paracellular permeability in piglet jejunum. Tonic release of enteric neurotransmitters regulates paracellular permeability in the fed state, and cholinergic stimulation restores fasting-induced elevations in paracellular permeability to fed levels.


Subject(s)
Animal Nutritional Physiological Phenomena , Enteric Nervous System/physiology , Intestinal Absorption/physiology , Jejunum/innervation , Jejunum/physiology , Animals , Atropine/pharmacology , Bicarbonates/metabolism , Biological Transport/drug effects , Biological Transport/physiology , Body Weight , Eating/physiology , Enteric Nervous System/drug effects , Fasting/physiology , Ganglionic Blockers/pharmacology , Intestinal Mucosa/innervation , Intestinal Mucosa/metabolism , Jejunum/metabolism , Mecamylamine/pharmacology , Membrane Potentials/drug effects , Membrane Potentials/physiology , Neurotransmitter Agents/metabolism , Parasympatholytics/pharmacology , Swine , Tetrodotoxin/pharmacology
2.
Dig Dis Sci ; 43(11): 2536-41, 1998 Nov.
Article in English | MEDLINE | ID: mdl-9824147

ABSTRACT

Infection with enterotoxigenic E. coli (ETEC) induces secretory diarrhea by stimulating net secretion of fluid and electrolytes. We tested the hypothesis that ETEC potentiates jejunal ion secretion induced by other agonists and also examined whether the soluble fiber psyllium ameliorates effects of ETEC-induced pathophysiology. Noninfected or ETEC-infected piglets were given oral electrolyte solution twice daily or electrolyte solution supplemented with psyllium for 48 hr. Jejunal tissues were mounted in flux chambers and basal and stimulated ion transport responses, as reflected by short-circuit current (I(SC)) were measured. The severity of ETEC-induced diarrhea was reduced by psyllium. I(SC) responses to carbachol and 5-hydroxytryptamine were greater in tissues from infected piglets compared with noninfected controls or infected piglets given psyllium. These results suggest that psyllium ameliorates ETEC-induced diarrhea and prevents the enhanced secretory responses to calcium-mediated agonists that occur in ETEC-infected piglet jejunum.


Subject(s)
Cathartics/therapeutic use , Enterotoxins/toxicity , Escherichia coli Infections/drug therapy , Escherichia coli , Feces , Jejunum/drug effects , Psyllium/therapeutic use , Analysis of Variance , Animals , Animals, Suckling , Cathartics/pharmacokinetics , Diarrhea/drug therapy , Diarrhea/physiopathology , Drug Evaluation, Preclinical , Escherichia coli Infections/physiopathology , Ion Transport/drug effects , Jejunum/metabolism , Nutritional Status , Psyllium/pharmacokinetics , Swine
3.
Cell Tissue Res ; 283(2): 209-13, 1996 Feb.
Article in English | MEDLINE | ID: mdl-8593650

ABSTRACT

Antibodies raised against the cystic fibrosis transmembrane regulator protein (CFTR) were used to localize CFTR in intestinal tissues of piglets and mice. Positive staining for CFTR was detected in goblet cells of both species. A second population of epithelial cells of unknown phenotype was also labeled by anti-CFTR antibodies. The labeling pattern was abolished by preincubation of anti-CFTR antibodies with the immunogen or when non-immune IgG was used in place of anti-CFTR antibodies. These results support other studies that suggest that alterations in goblet cell function may be involved in the intestinal abnormalities associated with cystic fibrosis.


Subject(s)
Cystic Fibrosis Transmembrane Conductance Regulator/analysis , Intestinal Mucosa/chemistry , Animals , Cystic Fibrosis/pathology , Immunoenzyme Techniques , Mice , Swine
4.
Am J Vet Res ; 57(2): 211-5, 1996 Feb.
Article in English | MEDLINE | ID: mdl-8633810

ABSTRACT

OBJECTIVE: To examine the role of prostaglandins and enteric nerves in mediating intestinal secretion induced by enterotoxigenic Escherichia coli heat-stable enterotoxin (STa) in pig jejunum and distal portion of the colon. ANIMALS: Two- to 3-week-old suckling crossbred pigs were studied. DESIGN: Changes in ion transport in response to mucosal addition of E coli STa to jejunal and colonic tissues were studied in the presence and absence of inhibitors. PROCEDURE: Flat sheets of muscle-stripped proximal portions of the jejunum and distal portions of the colon were mounted in Ussing chambers equipped to measure changes in short-circuit current (Isc), a measure of active ion transport. Tissues were exposed to 200 ng of STa/ml administered to mucosal solutions, and subsequent changes in Isc were recorded. RESULTS: In control tissues, changes in Isc induced by STa in the distal colon were significantly greater (21.4 +/- 4 muA/cm2) than those observed in the jejunum (14.0 +/- 2 muA/cm2). When either segment was exposed to the neurotoxin, tetrodotoxin, or to the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine-methyl ester, Isc responses to STa were unchanged, suggesting no involvement of submucosal nerves in mediating STa-induced secretion. When tissues from the distal portion of the colon and jejunum were pretreated with piroxicam, a prostaglandin synthesis inhibitor, the STa-induced Isc response was significantly reduced by 52 and 57%, respectively. CONCLUSIONS: These results indicate that the pig jejunum and distal portion of the colon are sensitive to the secretory actions of enterotoxigenic E coli STa, and that the responses are mediated, in part, by release of prostaglandins.


Subject(s)
Bacterial Toxins/toxicity , Colon/metabolism , Enteric Nervous System/physiology , Enterotoxins/toxicity , Jejunum/metabolism , Prostaglandins/physiology , Swine/metabolism , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Arginine/analogs & derivatives , Arginine/pharmacology , Bacterial Toxins/metabolism , Colon/drug effects , Enterotoxins/metabolism , Enzyme Inhibitors/pharmacology , Escherichia coli Proteins , Jejunum/drug effects , NG-Nitroarginine Methyl Ester , Nitric Oxide Synthase/antagonists & inhibitors , Piroxicam/pharmacology , Prostaglandins/metabolism , Tetrodotoxin/pharmacology
5.
Am J Physiol ; 267(1 Pt 2): R156-63, 1994 Jul.
Article in English | MEDLINE | ID: mdl-8048618

ABSTRACT

Three-week-old piglets were used to study the effects of short-term fasting on jejunal ion transport. A 48-h fast significantly reduced mucosal weight, villus height, and crypt depth. Fasting increased basal short-circuit current (Isc), which reflects active ion transport, and total tissue conductance (Gt) of muscle-stripped jejunal sheets mounted in Ussing chambers. Increases in Isc evoked by carbachol, serotonin, histamine, prostaglandin E2, or Escherichia coli heat-stable enterotoxin were significantly greater in the fasted piglets. Isc responses to mucosal D-glucose were also enhanced by the fast. Under basal conditions, unidirectional and net fluxes of Na+ and Cl-, as well as serosal-to-mucosal inulin fluxes, were significantly increased in fasted piglets. In fed piglets, carbachol increased net Cl- secretion by stimulating serosal-to-mucosal Cl- flux; Gt was not affected. In fasted piglets, carbachol increased net Cl- secretion by inhibiting mucosal-to-serosal fluxes with no effect on serosal-to-mucosal fluxes. In addition, carbachol significantly inhibited mucosal-to-serosal Na+ fluxes and reduced Gt in this group. Thus a 48-h fast increased unidirectional and net ion fluxes in piglet jejunum and enhanced ion transport responses to secretory agonists. The mechanism by which carbachol stimulated net Cl- secretion was also altered by the fast. These results suggest that the absence of luminal nutrition changes the ion transport characteristics of the jejunal epithelium.


Subject(s)
Fasting/physiology , Jejunum/metabolism , Animals , Animals, Newborn , Bicarbonates/pharmacology , Biological Transport , Body Weight , Carbachol/pharmacology , Chlorides/metabolism , Culture Media , Electrophysiology , Glucose/pharmacology , Intestinal Mucosa/anatomy & histology , Inulin/metabolism , Ions , Jejunum/anatomy & histology , Jejunum/physiology , Sodium/metabolism , Stimulation, Chemical , Swine
6.
Am J Physiol ; 266(3 Pt 1): G504-10, 1994 Mar.
Article in English | MEDLINE | ID: mdl-7513129

ABSTRACT

Polyclonal antibodies raised against purified bovine renal papillary amiloride-sensitive Na+ channels were used to localize Na(+)-channel proteins in mouse and piglet small intestine. Immunostaining using the avidin-biotin-peroxidase technique revealed epithelial Na(+)-channel epitopes localized to apical regions of villus enterocytes in jejunal tissues of both species. Anti-Na(+)-channel antibodies also stained apical borders of villus enterocytes in piglet ileum and apical borders of surface cells in the piglet distal colon. On immunoblots of jejunal, colonic, and renal tissues the anti-Na(+)-channel antibodies recognized one to three polypeptides of apparent molecular masses similar to those found in bovine renal epithelial Na(+)-channel protein (the 55-65, 110-116, and 150-kDa subunits). The antibodies also recognized a polypeptide in the 40- to 45-kDa range in mouse intestine, which is comparable to the 35- to 40-kDa subunit of a renal Na+ channel. The results demonstrate that epitopes comparable to those present in renal amiloride-sensitive Na+ channels are found in apical regions of absorptive epithelial cells in the mammalian small and large intestine.


Subject(s)
Amiloride/pharmacology , Intestinal Mucosa/metabolism , Sodium Channels/drug effects , Animals , Animals, Suckling , Blotting, Western , Immunohistochemistry/methods , Mice , Staining and Labeling , Swine , Tissue Distribution
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