title: Role of prostaglandins and enteric nerves in Escherichia coli heat-stable enterotoxin (STa)-induced intestinal secretion in pigs.
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.
  
  
  METHODS
  Two- to 3-week-old suckling crossbred pigs were studied.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
authors.affiliation: Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706, USA.
authors.forename: U L
authors.initials: UL
authors.lastname: Hayden
authors.forename: R N
authors.initials: RN
authors.lastname: Greenberg
authors.forename: H V
authors.initials: HV
authors.lastname: Carey
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001427:Bacterial Toxins / Q000378:metabolism / Q000633:toxicity*; D003106:Colon / Q000187:drug effects / Q000378:metabolism*; D017615:Enteric Nervous System / Q000502:physiology*; D004768:Enterotoxins / Q000378:metabolism / Q000633:toxicity*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D029968:Escherichia coli Proteins; D007583:Jejunum / Q000187:drug effects / Q000378:metabolism*; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010894:Piroxicam / Q000494:pharmacology; D011453:Prostaglandins / Q000378:metabolism / Q000502:physiology*; D013552:Swine / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001427:Bacterial Toxins; D004768:Enterotoxins; D004791:Enzyme Inhibitors; D029968:Escherichia coli Proteins; D011453:Prostaglandins; C034151:heat stable toxin (E coli); D010894:Piroxicam; D013779:Tetrodotoxin; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester