title: Heat stress increases the effectiveness of early ischemic preconditioning in spinal cord protection.
abstract: OBJECTIVE
  This study was aimed to test the hypothesis that the combination of heat stress and early ischemic preconditioning (IP) applied before aortic occlusion would be protective against spinal cord ischemic injury.
  
  
  METHODS
  Thirty Whister-Albino rats were randomly divided into three groups. In group 1 (n=10), aorta was clamped just distal to the left renal artery and above the iliac bifurcation for 45 min. Group 2 (n=10) had 5 min of transient aortic occlusion and 30 min later underwent an additional 45 min. In group 3 (n=10), animals were heated to 41 degrees C and maintained at this temperature for 15 min. Twenty-four hours later, this hyperthermia pretreated group underwent the same early IP model of aortic occlusion. Neurologic status was assessed on postoperative 24 and 48 h by using the 15-point neurologic performance scale. Spinal cords were harvested for histopathological grading (1-4) and evaluated for the presence of heat shock protein-ubiquitin staining.
  
  
  RESULTS
  At 24 and 48 h, the mean neurologic performance scores of the group 1 were found to be significantly lower than those of groups 2 and 3. Although the neurologic assessment of rats performed on the 24h did not reveal statistically significant difference between groups 2 and 3 (P=0.069); on 48 h, the mean neurologic scores of the group 3 were significantly higher than those of group 2 (P=0.005). At 48 h, a delayed neurologic deterioration was seen in groups 1 and 2 when compared to the results obtained at 24h. Histologic evaluation correlated well with the neurologic outcome with the least cellular damage in group 3. There were six rats with ubiquitin expression and this was detected only in animals pretreated with sublethal heat stress.
  
  
  CONCLUSIONS
  An early IP model with a short reperfusion interval does not give the minimal required time for the HSPs expression and is associated with a delayed neurologic deterioration. Neuroprotection provided by heat stress combined with an early IP model lasts up to 48 h and heat shock protein-ubiquitin induction may be responsible in this phenomenon.
authors.affiliation: Department of Cardiovascular Surgery, Istanbul University, GATA, Haydarpasa Military Training Hospital, Istanbul 84390, Turkey. dr_murat_basaran@yahoo.com
authors.forename: Murat
authors.initials: M
authors.lastname: Basaran
authors.forename: Eylul
authors.initials: E
authors.lastname: Kafali
authors.forename: Omer
authors.initials: O
authors.lastname: Sayin
authors.forename: Murat
authors.initials: M
authors.lastname: Ugurlucan
authors.forename: Melih Hulusi
authors.initials: MH
authors.lastname: Us
authors.forename: Cicek
authors.initials: C
authors.lastname: Bayindir
authors.forename: Ahmet Turan
authors.initials: AT
authors.lastname: Yilmaz
authors.forename: Enver
authors.initials: E
authors.lastname: Dayioglu
mesh_terms: D000818:Animals; D005260:Female; D018882:Heat Stress Disorders; D006614:Hindlimb; D007150:Immunohistochemistry / Q000379:methods; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D023421:Models, Animal; D009068:Movement; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion; D013116:Spinal Cord / Q000098:blood supply* / Q000737:chemistry; D020760:Spinal Cord Ischemia / Q000378:metabolism / Q000517:prevention & control*; D025801:Ubiquitin / Q000032:analysis
chemical_list: D025801:Ubiquitin