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(Stroke. 2008;39:983.)
© 2008 American Heart Association, Inc.

Original Contributions

Ischemic Postconditioning Protects Against Global Cerebral Ischemia/Reperfusion-Induced Injury in Rats

Jing-ye Wang, MD; Jia Shen, MS; Qin Gao, PhD; Zhi-guo Ye, MS; Shui-you Yang, BS; Hua-wei Liang, PhD; Iain C. Bruce, PhD; Ben-yan Luo, MD Qiang Xia, PhD

From the Department of Neurology, First Affiliated Hospital (J.-y.W., B.-y.L.); the Department of Physiology (J.-y.W., J.S., Q.G., Z.-g.Y., H.-w.L., I.C.B., Q.X.); and the Morphology Center (S.-y.Y.), Zhejiang University School of Medicine, Hangzhou, China.

Correspondence to Ben-yan Luo, MD, Department of Neurology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. E-mail luobenyan{at}zju.edu.cn, or Qiang Xia, PhD, Department of Physiology, Zhejiang University School of Medicine, 388 Yuhangtang Road, Hangzhou 310058, China. E-mail xiaqiang@zju.edu.cn

Background and Purpose— 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.

Key Words: brain ischemia • ischemic postconditioning • rats • reperfusion injury

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