title: Intestinal nitric oxide synthase activity changes during experimental colon obstruction.
abstract: OBJECTIVE
  The experiments in this study were designed to follow the time course of nitric oxide (NO) synthesis in the large bowel during acute mechanical ileus.
  
  
  METHODS
  Occlusion of the mid-transverse colon was maintained for 420 min in anesthetized dogs. Strain-gauge transducers were used to analyze motility changes on the hepatic and lienal flexures, respectively. Constitutive NO synthase (cNOS) and inducible NOS (iNOS) activities were determined in tissue biopsies, and plasma nitrite/nitrate (NOx) level was measured in the portal blood. Following completion of the baseline studies, the animals were treated with either 7-nitroindazole (7-NI, selective neuronal NOS inhibitor), or N-nitro-L-arginine (NNA, non-selective NOS inhibitor).
  
  
  RESULTS
  In the sham-operated group the cNOS activities differed significantly in the oral and aboral tissue samples (oral: 102.9; versus aboral: 62.1 fmol/mg protein/min). The obstruction elicited a significant increase in portal NOx and elevated tissue inducible NO synthase (iNOS) activity. NNA treatment decreased the motility index in both intestinal segments for 60 min, but 120 min later the motility index was significantly elevated (2.5-fold increase in the oral part, and 1.8-fold enhancement in the aboral segment, respectively). Treatment with 7-NI decreased the cNOS activity in the oral and aboral parts by approximately 40% and 70%, respectively, and suppressed the motility increase in the aboral colon segment.
  
  
  CONCLUSIONS
  The motility of the colon was either significantly increased or decreased, depending on the type and selectivity of the NOS inhibitor compounds applied. NO of neuronal origin is a transmitter that stimulates peristaltic activity; but an increased iNOS/nNOS ratio significantly moderates the obstruction-induced motility increase.
authors.affiliation: Department of Surgery, Szent-Györgyi Albert Medical and Pharmaceutical Centre, University of Szeged, Hungary.
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Palásthy
authors.forename: József
authors.initials: J
authors.lastname: Kaszaki
authors.forename: György
authors.initials: G
authors.lastname: Lázár
authors.forename: Sándor
authors.initials: S
authors.lastname: Nagy
authors.forename: Mihály
authors.initials: M
authors.lastname: Boros
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003108:Colonic Diseases / Q000097:blood / Q000201:enzymology* / Q000503:physiopathology; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005769:Gastrointestinal Motility; D007415:Intestinal Obstruction / Q000097:blood / Q000201:enzymology* / Q000503:physiopathology; D007420:Intestine, Large / Q000201:enzymology*; D009566:Nitrates / Q000097:blood; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism; D009573:Nitrites / Q000097:blood; D019335:Nitroarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D009566:Nitrates; D009573:Nitrites; D019335:Nitroarginine; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II