• Xu-Dong Ding, Ning-Ning Zheng, Yan-Yan Cao, Guang-Yi Zhao, and Ping Zhao.
• a Department of Anesthesiology, Shengjing Hospital , China Medical University , Shenyang , China.
• Int. J. Neurosci. 2016 Jan 1; 126 (3): 249-56.

Background/AimsTo investigate the protection effect of dexmedetomidine preconditioning on global cerebral ischemic injury following asphyxial cardiac arrest (CA) in rats.MethodsSeventy-two rats were randomly assigned into three groups, sham group (no asphyxia), control group (asphyxia only), and dexmedetomidine preconditioned group (asphyxia + dexmedetomidine). Dexmedetomidine was administered 5 minutes before an 8 min of asphyxia. Rats were resuscitated by a standardized method. Blood O(2) and CO(2) partial pressures were, pH, base excess (BE), and blood glucose concentration measured before asphyxial CA and 1 h after resuscitation. Neurological deficit score (NDS) was measured at 12, 24, 48, and 72 h after CA. Histopathologic changes in the hippocampal region were observed by H&E staining and histopathologic damage score. Ultrastructural morphology was observed by transmission electron microscopy. HIF-1 and VEGF expression were measured by immunostaining of serial sections obtained from brain tissue.ResultsAsphyxial CA -induced global cerebral ischemic decreased PaO(2), pH, BE and increased PaCO(2), blood glucose. Dexmedetomidine preconditioning improved neurologic outcome, which was associated with reduction in histopathologic injury measured by H&E staining, the histopathologic damage score and electron microscopy. Dexmedetomidine preconditioning also elevated HIF-1α and VEGF expression after global cerebral ischemia following asphyxial CA.ConclusionDexmedetomidine preconditioning protected against cerebral ischemic injury and was associated with upregulation of HIF-1α and VEGF expression.

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