Objective To investigate the beneficial effects and possible mechanisms of intrathecal injection of dexmedetomidine (DEX) in protection of spinal cord ischemia-reperfusion injury.Methods Spinal cord ischemia-reperfusion injury was induced in rabbits by infrarenal aortic occlusion for 30 minutes.Twenty-four rabbits were randomly divided into four groups:sham group,I/R group,DEX group (1 μg/kg dexmedetomidine by intrathecal injection),DEX + ATIP group (1 μg/kg dexmedetomidine and 0.5 μg/kg atipamezole (ATIP) by intrathecal injection).Physiological indices were assessed and motor neurons in the ventral gray matter were counted by histological examination.The expression of total extracellular signal-related kinase (t-ERK),phospho-extracellular signal-related kinase (p-ERK),and caspase 3 were assessed by Western blotting and real-time polymerase chain reaction (RT-PCR).The water content in spines was also measured.Results Intrathecal injection of dexmedetomidine minimized the neuromotor dysfunction and histopathological deficits(F =14.32,P ＜ 0.05) and attenuated the influences of peroxidation at 24 hours after spinal cord ischemia-reperfusion injury.The physical indices during experiment were comparable among all groups.In addition,intrathecal injection of dexmedetomidine reduced the excessive expression of caspase 3 mediated by ERK signal pathway(F =15.45,P ＜ 0.05).Conclusions Pre-emptive intrathecal injection of dexmedetomidine produced beneficial effects on spinal cord after spinal cord ischemia-reperfusion injury in a rabbit model of transient aortic occlusion.This beneficial effect was partly attributed to the inhibition of caspase 3 mediated by ERK signal pathway,which represents a potential therapeutic approach to mitigate spinal cord injury after aortic occlusion.