title: Ischemic preconditioning by selective occlusion of the pulmonary artery in rats.
abstract: OBJECTIVE
  To evaluate the effect of lung ischemic preconditioning (IPC) on normothermic ischemia/reperfusion (I/R) injury in a rat model, quantifying the production of reactive oxygen species.
  
  
  METHODS
  Forty-seven male Wistar rats were randomized into four groups: control, sham, I/R and IPC. Control group animals were anesthetized and killed by decapitation, after which pneumonectomy was performed and the left lungs were stored in liquid nitrogen. Sham, IPC and I/R group rats were anesthetized, tracheostomized, ventilated, anticoagulated and submitted to left thoracotomy with dissection of the left pulmonary artery for clamping. Sham group rats underwent dissection of the left pulmonary artery, I/R group rats underwent 30 min of total hilar clamping, and IPC group rats underwent 5-min clamping of the left pulmonary artery followed by 30 min of total hilar clamping. Lungs were reperfused for 90 min and ventilated with the same parameters, with additional positive end-expiratory pressure of 1 cmH2O. Hemodynamic and blood gas values were obtained prior to thoracotomy, prior to total hilar clamping, after 30 min of reperfusion and after 90 min of reperfusion. Lipid peroxidation was determined by measuring levels of thiobarbituric acid reactive substances.
  
  
  RESULTS
  There were no significant differences among the groups in terms of the levels of thiobarbituric acid reactive substances. Nor were there any significant differences among the sham, I/R and IPC groups in terms of arterial oxygen tension, arterial carbon dioxide tension or hemodynamic values.
  
  
  CONCLUSIONS
  In an in situ I/R rat model, 5-min IPC of the left pulmonary artery does not attenuate I/R injury.
authors.affiliation: Fundação Faculdade Federal de Ciências Médicas de Porto Alegre, Porto Alegre, Brasil.
authors.forename: Eduardo Sperb
authors.initials: ES
authors.lastname: Pilla
authors.forename: Giovani Schirmer
authors.initials: GS
authors.lastname: Vendrame
authors.forename: Pablo Gerardo
authors.initials: PG
authors.lastname: Sánchez
authors.forename: Gustavo
authors.initials: G
authors.lastname: Grun
authors.forename: Eduardo
authors.initials: E
authors.lastname: Fontena
authors.forename: Luiz Alberto
authors.initials: LA
authors.lastname: Forgiarini
authors.forename: Norma Anair Possa
authors.initials: NA
authors.lastname: Marroni
authors.forename: Cristiano Feijó
authors.initials: CF
authors.lastname: Andrade
authors.forename: Paulo Francisco Guerreiro
authors.initials: PF
authors.lastname: Cardoso
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D035061:Control Groups; D004195:Disease Models, Animal; D019194:Ischemic Preconditioning / Q000379:methods*; D015227:Lipid Peroxidation / Q000502:physiology; D008168:Lung / Q000098:blood supply* / Q000737:chemistry; D008297:Male; D009926:Organ Preservation / Q000379:methods; D011651:Pulmonary Artery / Q000503:physiopathology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000517:prevention & control*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances