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Does remote ischemic preconditioning prevent delayed hippocampal neuronal death following transient global cerebral ischemia in rats?

Department of Cardiothoracic Surgery, Sir Charles Gairdner Hospital, School of Surgery, University of Western Australia, Perth, Australia

Arul Bala

Department of Cardiothoracic Surgery, Sir Charles Gairdner Hospital, School of Surgery, University of Western Australia, Perth, Australia

Kym Campbell

Centre for Neuromuscular and Neurological Disorders, University of Western Australia, Perth, Australia

Bruno Meloni

Centre for Neuromuscular and Neurological Disorders, University of Western Australia, Perth, Australia

Yves d'Udekem

Cardiac Surgery Unit, Royal Children's Hospital, University of Melbourne, Melbourne, Australia

Igor E. Konstantinov

Department of Cardiothoracic Surgery, Sir Charles Gairdner Hospital, School of Surgery, University of Western Australia, Perth, Australia, konstantinov.igor{at}alumni.mayo.edu, Cardiac Surgery Unit, Royal Children's Hospital, University of Melbourne, Melbourne, Australia

Objective: To 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).

Method: Animals 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.

Results: There 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). Conclusion: Second window of the RIPC does not prevent hippocampal CA1 neuronal death at 7 days after transient global cerebral ischemia.

Key Words: Global cerebral ischemia • remote ischemic preconditioning • CA1 neurons • hippocampus

This version was published on May 1, 2009

Perfusion, Vol. 24, No. 3, 207-211 (2009)
DOI: 10.1177/0267659109346902


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