title: Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats.
abstract: OBJECTIVE
  Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats.
  
  
  METHODS
  Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats. The animals underwent postconditioning consisting of 3 cycles of 15-second/15-second (Post-15/15), 30-second/30-second (Post-30/30), or 60-second/15-second (Post-60/15) reperfusion/reocclusion or 15-second/15-second reperfusion/reocclusion applied after a 45-second reperfusion (Post-45-15/15).
  
  
  RESULTS
  Ten minutes of ischemia and 7 days of reperfusion destroyed 85.8% of CA1 hippocampal neurons and 64.1% of parietal cortical neurons. Three cycles of Post-15/15, Post-30/30, and Post-45-15/15 reperfusion/reocclusion markedly reduced neuronal loss after 7 days or 3 weeks of reperfusion and diminished the deficiency in spatial learning and memory. After reperfusion, a period of hyperperfusion followed by hypoperfusion was observed, both of which were blocked by postconditioning. The cytosolic level of cytochrome c increased significantly after 48 hours of reperfusion, and this was inhibited by Post-15/15, Post-30/30, and Post-45-15/15. However, 3 cycles of 60-second/15-second reperfusion/reocclusion failed to protect against neuronal damage, behavioral deficit, or cytochrome c translocation.
  
  
  CONCLUSIONS
  Our data provide the first evidence that an appropriate ischemic postconditioning strategy has neuroprotective effects against global cerebral ischemia/reperfusion injury and a consequent behavioral deficit and that these protective effects are associated with its ability to improve disturbed cerebral blood flow and prevent cytochrome c translocation.
authors.affiliation: Department of Neurology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: Jing-ye
authors.initials: JY
authors.lastname: Wang
authors.forename: Jia
authors.initials: J
authors.lastname: Shen
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Zhi-guo
authors.initials: ZG
authors.lastname: Ye
authors.forename: Shui-you
authors.initials: SY
authors.lastname: Yang
authors.forename: Hua-wei
authors.initials: HW
authors.lastname: Liang
authors.forename: Iain C
authors.initials: IC
authors.lastname: Bruce
authors.forename: Ben-yan
authors.initials: BY
authors.lastname: Luo
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology* / Q000523:psychology; D002452:Cell Count; D002560:Cerebrovascular Circulation; D045304:Cytochromes c / Q000378:metabolism; D019610:Cytoprotection; D003600:Cytosol / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D019194:Ischemic Preconditioning / Q000379:methods; D008297:Male; D018782:Maze Learning; D008568:Memory; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010296:Parietal Lobe / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology* / Q000523:psychology; D013550:Swimming; D013997:Time Factors
chemical_list: D045304:Cytochromes c