title: Protective effect of exogenous nitric oxide on the renal function and inflammatory response in a model of ischemia-reperfusion.
abstract: BACKGROUND
  Tissue subjected to a period of ischemia undergoes morphological and functional damage that increases during the reperfusion phase. The aim of the present work was to assess the possible improvement induced by exogenous administration of nitric oxide (NO) on renal injury and inflammatory reaction in an experimental animal model of renal ischemia-reperfusion (I-R).
  
  
  METHODS
  Ischemia was achieved by ligation of the left arteria and vein for 60 min, followed first by contralateral nephrectomy and then reestablishment of blood flow. Molsidomine, used as an NO donor, was administered by systemic injection 30 min before reperfusion. The effect of molsidomine was compared with the effect of hydralazine, a non-NO donor hypotensive agent.
  
  
  RESULTS
  Treatment with molsidomine improved the renal dysfunction (increase in plasma creatinine and urea levels) caused by I-R. Moreover, molsidomine blunted the enhanced production of proinflammatory cytokines (tumor necrosis factor [TNF]-alpha and interleukin [IL] 1alpha), the increase in tissular levels of superoxide anions and oxygen free radical scavengers, and the neutrophilic infiltration observed in the ischemic kidney. One hundred percent survival was achieved in the group of animals treated with the NO donor, whereas the groups of animals undergoing I-R that did not receive molsidomine showed a 40% mortality from the second day after reperfusion.
  
  
  CONCLUSIONS
  The present work demonstrated that systemic treatment with an NO donor before reperfusion improved renal function and diminished inflammatory responses in a kidney subjected to an I-R process.
authors.affiliation: Departamento de Cirugia, Universidad de Salamanca, Spain.
authors.forename: F J
authors.initials: FJ
authors.lastname: Garcia-Criado
authors.forename: N
authors.initials: N
authors.lastname: Eleno
authors.forename: F
authors.initials: F
authors.lastname: Santos-Benito
authors.forename: J J
authors.initials: JJ
authors.lastname: Valdunciel
authors.forename: M
authors.initials: M
authors.lastname: Reverte
authors.forename: F S
authors.initials: FS
authors.lastname: Lozano-Sánchez
authors.forename: M D
authors.initials: MD
authors.lastname: Ludeña
authors.forename: A
authors.initials: A
authors.lastname: Gomez-Alonso
authors.forename: J M
authors.initials: JM
authors.lastname: López-Novoa
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D016207:Cytokines / Q000097:blood; D016166:Free Radical Scavengers / Q000378:metabolism; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D007677:Kidney Function Tests; D008297:Male; D009393:Nephritis / Q000473:pathology*; D009569:Nitric Oxide / Q000494:pharmacology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012079:Renal Circulation / Q000502:physiology; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D013481:Superoxides / Q000378:metabolism; D016019:Survival Analysis
chemical_list: D016207:Cytokines; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D013481:Superoxides; D009569:Nitric Oxide; D009195:Peroxidase