실험연구 : 백서의 척수허혈시 허혈시간에 따른 신경손상과 유전자발현의 변화에 관한 연구

Background: Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Many papers have been published on this topic but without a clear consensus on the best way of minimizing the problem. For the further study of preventing neurological injury after spinal ischemia, the proper animal model is necessary. In this study we compared spinal ischemia time on neurologic and histopathologic outcome, and inflammatory gene expression in transient spinal ischemia. Methods : Rats were anesthetized with halothane, and divided into 4 groups: 12.5 minutes of spinal ischemia (Group 1), 15 minutes of spinal ischemia (Group 2), 17.5 minutes of spinal ischemia (Group 3), and 20 minutes of spinal ischemia (Group 4). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. After spinal ischemia neurologic scores were assessed after 1, 3, 6, and 24 hours. After 24 hours, rats were euthanized and spinal cords were removed for histopathologic assessment and an assay of TNF- a and IL-1 mRNA. Results : The neurologic scores worsened according to the ischemia time. The histopathologic scores correlated well with the neurologic scores. The TNF- a and IL-1 mRNA expression results of group 2 were larger than those of group 1. There were no significant differences between group 2, group 3, and group 4. Conclusions: Inflammatory gene expressions are increased during transient spinal ischemia. After 15 minutes of ischemia, no further increase of mRNA expression was shown. The 15 minutes of spinal ischemia was sufficient for the spinal ischemic study in rats. (Korean J Anesthesiol 2000; 38: 904~ 909)