• Young-Tae Jeon, Jung-Won Hwang, Young-Jin Lim, Seon-Kyoung Park, and Hee-Pyoung Park.
• Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul 110-744, South Korea.
• J Neurosurg Anesthesiol. 2013 Apr 1;25(2):184-90.

BackgroundWe designed this study to determine whether a combination of dexmedetomidine and sevoflurane postconditioning provides additive neuroprotection in a rat model of transient global cerebral ischemia.MethodsForty rats were randomly allocated to 4 groups. Control group (group C, n=10) received no treatment. Dexmedetomidine group (group D, n=10) received dexmedetomidine of 100 μg/kg intraperitoneally 30 minutes before ischemia. Sevoflurane postconditioning group (group P, n=10) underwent 2 sevoflurane inhalations after ischemia. Each inhalation consisted of 5 minutes of 2.5% sevoflurane and a subsequent washout time of 10 minutes. Sevoflurane postconditioning plus dexmedetomidine group (group PD, n=10) received received dexmedetomidine and 2 sevoflurane inhalations 30 minutes before ischemia and after ischemia, respectively. In all the groups, ischemia was induced by a bilateral common carotid artery occlusion plus hemorrhagic hypotension and was maintained for 8 minutes. Histologic outcomes and apoptosis-related proteins were measured 7 days after ischemia in the CA1 area of the rat hippocampus.ResultsGroups D, P, and PD contained more viable cells and less apoptotic cells in the hippocampal CA1 area than group C (P<0.01). There was a significant difference in the Bax and Bcl-2 expression between group C and other groups (P<0.05). But the number of viable and apoptotic cells, and the Bax and Bcl-2 expression were not statistically different between group D or P and group PD.ConclusionsA combination of preischemic dexmedetomidine and sevoflurane postconditioning provides no additional neuroprotective benefit over preischemic dexmedetomidine or sevoflurane postconditioning alone.

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