title: Protective effects of ischemic preconditioning on lung ischemia reperfusion injury: an in-vivo rabbit study.
abstract: BACKGROUND
  The goal of this study was to determine the effect of ischemic preconditioning on the extent of normothermic lung ischemia reperfusion injury in rabbits in vivo.
  
  
  METHODS
  Thirty male Japanese white rabbits were randomized into two groups. Fifteen rabbits were treated with ischemic preconditioning (their left lung hilus clamped for 10 minutes and released for 15 minutes (group IP)). Fifteen rabbits were not treated with ischemic preconditioning (group C). Then the left lung hilus of both groups were occluded for 60 minutes and reperfused for 60 minutes. Mean arterial pressure, mean pulmonary artery pressure, and core temperature were recorded. Femoral artery blood samples and lung tissue samples were collected after ischemic preconditioning and after 60 minutes of reperfusion.
  
  
  RESULTS
  The lung tissue showed little injury after ischemic preconditioning. After 60 minutes of reperfusion, the angiotensin II (A II) and arterial oxygen tension (PaO2) levels in group IP were significantly higher than those in group C, mean pulmonary artery pressure in group IP was significantly lower than that in group C, the wet/dry ratio and malondialdehyde content of lung tissue in group IP was significantly lower than that in group C, the superoxide dismutase contents of lung tissue in group IP was significantly higher than that in group C, and histological findings showed less damage in group IP than in group C.
  
  
  CONCLUSIONS
  Lung ischemic preconditioning could reduce normothermic rabbit lung ischemia-reperfusion injury. The possible mechanisms are increased production of endogenous A II and reduced formation of oxygen free radicals during lung ischemia for 60 minutes followed by reperfusion for 60 minutes.
authors.affiliation: Department of Cardiothoracic Surgery, Xiangya Hospital, Hunan Medical University, Changsha, PR China.
authors.forename: G
authors.initials: G
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Chen
authors.forename: E
authors.initials: E
authors.lastname: Lu
authors.forename: T
authors.initials: T
authors.lastname: Hu
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D019194:Ischemic Preconditioning; D008168:Lung / Q000098:blood supply* / Q000201:enzymology; D008171:Lung Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D011817:Rabbits; D011897:Random Allocation; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000804:Angiotensin II; D008315:Malondialdehyde; D013482:Superoxide Dismutase