title: Clinically relevant thermal preconditioning attenuates ischemia-reperfusion injury.
abstract: BACKGROUND
  Thermal preconditioning has previously been shown to attenuate ischemia-reperfusion induced injuries, possible due to increased expression of heat shock proteins (HSP). The model of thermal preconditioning used, however, was not clinically relevant as preconditioning was to 41 degrees C, leading to cellular damage. Our aim was thus to establish a novel and clinically applicable method of preconditioning.
  
  
  METHODS
  Twenty-six male Sprague-Dawley rats were split into three groups (nine control, nine ischemia-reperfusion, and eight preconditioned followed by ischemia-reperfusion). To precondition the animals, they were anesthetized and, using a water bath, their core temperature was raised by 1 degrees C for 15 min once a day for five successive days. I/R injury consisted of 30 min of aortic cross-clamping followed by 120 min of reperfusion; control animals had a laparotomy only. Indicators of lung injury were tissue myeloperoxidase, broncho-alveolar lavage protein concentration, and tissue edema. Tissue heat shock protein expression was detected by Western blot analysis.
  
  
  RESULTS
  Lower torso ischemia-reperfusion causes significant lung injury versus control, with raised levels of myeloperoxidase 4.53 iu/g to 7.88 iu/g (P < 0.05), raised B.A.L. protein concentration 419 microg/ml to 684 microg/ml (P < 0.05) and altered wet dry ratio 4.63 to 5.50. Clinically relevant thermal preconditioning attenuates all of these parameters back to control levels: myeloperoxidase 3.87 iu/g (P < 0.05 vs I/R), B.A.L. to 284 microg/ml (P < 0.01 vs I/R) and wet dry ratio to 4.44 (P < 0.05 vs I/R). Western blot demonstrated increased expression of H.S.P. 72 in the preconditioned group versus control and I/R alone. Western blot demonstrated increased expression of HSP72 in the preconditioned group vs control and I/R alone.
  
  
  CONCLUSIONS
  We conclude that clinically applicable thermal preconditioning can attenuate ischemia-reperfusion induced lung injury, possibly through increased expression of HSP72.
authors.affiliation: Department of Surgery, Royal College of Surgeons of Ireland, Beaumont Hospital, 9 Dublin, Republic of Ireland. paulhmccormick@hotmail.com
authors.forename: P H
authors.initials: PH
authors.lastname: McCormick
authors.forename: G
authors.initials: G
authors.lastname: Chen
authors.forename: S
authors.initials: S
authors.lastname: Tlerney
authors.forename: C J
authors.initials: CJ
authors.lastname: Kelly
authors.forename: D J
authors.initials: DJ
authors.lastname: Bouchier-Hayes
mesh_terms: D000818:Animals; D001011:Aorta; D015153:Blotting, Western; D001831:Body Temperature; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002199:Capillary Permeability; D003250:Constriction; D004487:Edema; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis; D006358:Hot Temperature; D019194:Ischemic Preconditioning; D008168:Lung / Q000098:blood supply* / Q000737:chemistry / Q000473:pathology; D008297:Male; D009929:Organ Size; D009195:Peroxidase / Q000032:analysis; D011506:Proteins / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D011506:Proteins; D009195:Peroxidase