title: Evaluating the potential role of nitric oxide as a mediator of hydrostatic edema mediated intestinal contractile dysfunction.
abstract: BACKGROUND
  Administration of L-nil, a selective inhibitor of inducible nitric oxide synthase (iNOS), improves ileus in an animal model of resuscitation induced intestinal edema. The purpose of this study was to elucidate the iNOS/nitric oxide (NO) signal transduction pathway in intestinal edema.
  
  
  METHODS
  Male Sprague Dawley rats were divided into two groups; CONTROL and RESUS+VH (edema, 80 cc/kg normal saline (resuscitation) with mesenteric venous hypertension). iNOS mRNA and protein, iNOS activity, NO tissue levels, soluble guanylyl cyclase (sGC) expression, and cyclic guanosine monophosphate (cGMP) levels were measured. As a functional endpoint, we evaluated intestinal contractile strength and frequency in L-nil treated animals.
  
  
  RESULTS
  Edema was associated with increased iNOS mRNA and protein expression without subsequent increases in iNOS activity or tissue NO levels. There was no significant change in sGC expression or increase in cGMP induced by edema. Administration of L-nil did not decrease edema development or preserve contractile strength, but increased contractile frequency.
  
  
  CONCLUSIONS
  Hydrostatic intestinal edema is not associated with increased iNOS activity or tissue NO levels. Administration of L-nil in edema increases intestinal contractile frequency. This may represent a potential mechanism for the amelioration of ileus seen with the administration of L-nil.
authors.affiliation: Department of Pediatric Surgery, University of Texas Medical School at Houston, Houston, Texas 77030, USA.
authors.forename: Shinil K
authors.initials: SK
authors.lastname: Shah
authors.forename: Hasen
authors.initials: H
authors.lastname: Xue
authors.forename: Fernando
authors.initials: F
authors.lastname: Jimenez
authors.forename: Alexander Y
authors.initials: AY
authors.lastname: Kots
authors.forename: Byung-Kwon
authors.initials: BK
authors.lastname: Choi
authors.forename: Karen S
authors.initials: KS
authors.lastname: Uray
authors.forename: Peter A
authors.initials: PA
authors.lastname: Walker
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: Natalia
authors.initials: N
authors.lastname: Velez
authors.forename: Randolph H
authors.initials: RH
authors.lastname: Stewart
authors.forename: Glen A
authors.initials: GA
authors.lastname: Laine
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
mesh_terms: D000818:Animals; D006152:Cyclic GMP / Q000378:metabolism*; D004487:Edema / Q000378:metabolism*; D005769:Gastrointestinal Motility; D006162:Guanylate Cyclase / Q000378:metabolism; D006874:Hydrostatic Pressure; D007150:Immunohistochemistry; D007410:Intestinal Diseases / Q000201:enzymology*; D008239:Lysine / Q000031:analogs & derivatives; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction
chemical_list: C090663:N(6)-(1-iminoethyl)lysine; D012333:RNA, Messenger; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D006162:Guanylate Cyclase; D006152:Cyclic GMP; D008239:Lysine