• Pankaj Saxena, Arul Bala, Kym Campbell, Bruno Meloni, Yves d'Udekem, and Igor E Konstantinov.
• Department of Cardiothoracic Surgery, Sir Charles Gairdner Hospital, School of Surgery, University of Western Australia, Perth, Australia.
• Perfusion. 2009 May 1; 24 (3): 207-11.

ObjectiveTo determine if remote ischemic preconditioning (RIPC) induced by transient limb ischemia is protective against delayed hippocampal neuronal death in rats undergoing transient global cerebral ischemia (GCI).MethodAnimals were randomized into 3 groups: Group I (Control, n = 5) underwent sham procedure, namely, general anesthesia x 2, without cerebral ischemia; Group II (RIPC + GCI, n = 5) was subjected to RIPC, induced by transient left hind limb ischemia under general anesthesia prior to GCI; Group III (GCI only, n = 5) underwent sham procedure under general anesthesia prior to GCI. Twenty-four hours after the RIPC or sham procedure, a transient GCI was induced for 8 minutes in Groups II and III by means of bilateral common carotid artery occlusion and hypotension. Hippocampal CA1 neurons were histologically examined at 7 days after ischemia.ResultsThere was no significant difference between the RIPC group and the ischemia only group. The number of neurons in the RIPC group were 0.90 (95% CI 0.20, 4.08) times the number in the ischemia group (p=0.89). The number of neurons in the RIPC group were 0.03 (95% CI 0.01, 0.10) times the number in the Control group (p=0.0001).ConclusionSecond window of the RIPC does not prevent hippocampal CA1 neuronal death at 7 days after transient global cerebral ischemia.

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