RESUMO
BACKGROUND: Although rare, paralysis secondary to spinal cord ischemia after aortic aneurysm surgery is a devastating complication. Many papers have been published on this topic but without a clear consensus on the best way of minimizing the problem. Mild hypothermia and lamotrigine have been neuroprotective in several models of cerebral ischemia. In this study we compared the effects of mild hypothermia and the lamotrigine on neurologic and histopathologic outcomes, and inflammatory gene expression in transient spinal ischemia. METHODS: Rats were anesthetized with halothane, and divided into 4 groups; the Sham-operated (S) group; the Normothermic ischemic (N) group; the Hypothermic ischemic (H) group; and the Lamotrigine- treated (L) group. Spinal ischemia was produced by induced hypotension and thoracic aortic cross clamping. After spinal ischemia neurologic scores were assessed at 1, 2, 3, 24, and 48 hours after reperfusion. After 48 hours the rats were euthanized and their spinal cords were removed for histopathologic assessment. Also, spinal cords were removed at 1, 3, and 48 hours after reperfusion for the assay of TNF-alpha, IL-1 mRNA. RESULTS: The neurologic scores of the H group were significantly lower than from the N group. There was no significant difference between the L group and the N group. The histopathologic scores in the H and L groups were significantly lower than in the N group, and the histopathologic scores of the L group were higher than those of the H group. The TNF-alpha and IL-1 gene expression was increased in the N group. In the H group, the gene expression was significantly less than in the N group. The L group was not significantly different than N group in gene expression. CONCLUSIONS: The inflammatory gene expressions were increased in transient spinal ischemia. Hypothermia was neuroprotective in transient spinal ischemia. However, the lamotrigine showed only partial neuroprotective effects in transient spinal ischemia.