title: In vitro effects of nonsteroidal anti-inflammatory agents and prostaglandins I2, E2, and F2alpha on contractility of taenia of the large colon of horses.
abstract: OBJECTIVE
  To determine the in vitro effect of various prostaglandins (PG) and nonsteroidal anti-inflammatory drugs (NSAID) on contractile activity of the large-colon taenia of horses.
  
  
  METHODS
  14 healthy horses.
  
  
  METHODS
  The taenia was collected from the ventral colon, cut into strips (2 X 10 mm), and mounted in a tissue bath system (20-ml capacity) that contained oxygenated Krebs buffer solution warmed to 37.5+/-0.5 C. After equilibration, incremental doses of PGE2, PGF2alpha, PGl2, flunixin meglumine, carprofen, ketoprofen, and phenylbutazone were added to the baths, and contractile activity was recorded. Magnitude of the response was calculated by comparing contractile activity before and after administration of the PG or NSAID to the tissue baths.
  
  
  RESULTS
  PGE2 and PGF2alpha, caused a significant increase in contractile activity, whereas PGI2 induced an inhibitory response. Activity of NSAID on contraction was predominantly inhibitory. At low concentrations, ketoprofen induced an excitatory effect, which then became inhibitory at high concentrations. Compared with the other NSAID, carprofen significantly reduced contractile activity at lower concentrations.
  
  
  CONCLUSIONS
  PGE2 and PGF2alpha appear to enhance contractility of large-colon taenia of horses, whereas PGI2 was inhibitory in the in vitro model. Administration of NSAID also inhibited contractility, with carprofen having the most potent effect.
  
  
  CONCLUSIONS
  Administration of NSAID in combination with liberation of endogenous PG may predispose horses to development of intestinal stasis and subsequent impaction.
authors.affiliation: Department of Surgical and Radiological Sciences, University of California, Davis 95616, USA.
authors.forename: L
authors.initials: L
authors.lastname: Van Hoogmoed
authors.forename: P C
authors.initials: PC
authors.lastname: Rakestraw
authors.forename: J R
authors.initials: JR
authors.lastname: Snyder
authors.forename: F A
authors.initials: FA
authors.lastname: Harmon
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002227:Carbazoles / Q000494:pharmacology; D003002:Clonixin / Q000031:analogs & derivatives / Q000494:pharmacology; D003106:Colon / Q000187:drug effects / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015237:Dinoprost / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D006736:Horses / Q000502:physiology*; D007213:Indomethacin / Q000494:pharmacology; D007660:Ketoprofen / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D010653:Phenylbutazone / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D002227:Carbazoles; D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; C014558:flunixin meglumine; D007660:Ketoprofen; D015237:Dinoprost; D011464:Epoprostenol; C007005:carprofen; D010653:Phenylbutazone; D015232:Dinoprostone; D003002:Clonixin; D007213:Indomethacin