RESUMEN
Aims: Dexmedetomidine, anα2adrenergicagonist, provides neuroprotection in various cerebral ischemia models and against anesthesia-related neurotoxicity. Dexmedetomidine also improves paraplegia induced by intrathecal morphine after short-term spinal ischemia. In this preliminary study, we investigated whether dexmedetomidine provides spinal protection against transient spinal ischemia in rats. Methodology: Adult male Sprague-Dawley rats were randomly divided into the following 3 groups: 1) intravenous infusion of 0.9% NaCl at a rate of 0.5 mL/h (control), 2) dexmedetomidine 1 μg/kg/h, and 3) intravenous infusion of 0.9% NaCl without spinal ischemia (sham). The rats received saline solution or dexmedetomidine 30 min before spinal cord ischemia and for 24 h. Spinal cord ischemia was induced by intra-aortic balloon occlusion combined with proximal arterial hypotension for 10 min. Ischemic injury was assessed by the neurological deficit score and by the number of viable motor nerve cells in the anterior spinal cord at 24 h of reperfusion. Results: The neurological deficit score was significantly lower in the dexmedetomidine group compared to the control group (p< 0.05). The number of viable motor nerve cells in the dexmedetomidine group was significantly greater than was that in the control group (p< 0.05), but was lower than was that in the sham group.Conclusion: Our findings suggest that continuous administration of dexmedetomidine ameliorates short-term neurological and histological outcomes induced by transient spinal cord ischemia and reperfusion in rats; thus, dexmedetomidine appears to protect the spinal as well as the brain.