Attenuation of spinal cord ischemia-reperfusion injury by specific α-2a receptor activation with dexmedetomidine.

摘要: Background Despite surgical adjuncts, paralysis remains a devastating complication after thoracoabdominal aortic interventions. Dexmedetomidine, selective α-2a agonist commonly used for sedation in the critical care setting, has been shown to have protective effects against ischemia-reperfusion injuries multiple organ systems. We hypothesized that treatment with dexmedetomidine would attenuate spinal cord injury via receptor activation. Methods Adult C57BL/6 mice underwent sternotomy, followed by occlusion of arch 4 minutes. Eight experimental received pretreatment intraperitoneal (25 μg/kg) and at 12-hour intervals reperfusion. control an equivalent amount 0.9% normal saline. Five same procedure atipamezole (250 μg/kg), antagonist. Functional analysis was obtained scored using Basso Mouse Scale Locomotion until 60 hours. All were euthanized Their cords removed en bloc stained hematoxylin eosin assess cytoarchitecture neuronal viability. Results Mice treated demonstrated preserved motor function compared ischemic controls antagonist addition agonist. differences group statistically significant from 24 hours through remainder experiment ( P Conclusions Treatment preserves viability cross-clamping. In addition, exhibited almost complete reversal effect administration atipamezole. Dexmedetomidine appears receptor-mediated agonism.