Abstract

BACKGROUND
Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. Anesthetic and ischemic preconditioning have been known to prevent ischemic injury. The purpose of this study was to elucidate the effects of sevoflurane and ischemic preconditioning (IPC) on neurologic outcome, DNA fragmentation and Bcl-2 protein gene expression in transient spinal ischemia. METHODS: Rats were anesthetized with enflurane or sevoflurane, divided by 5 groups: Sevoflurane group and enflurane group (13 minutes of ischemia), Control group, Rapid group, Delayed group (15 minutes of ischemia). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. Neurologic scores were assessed at the time of recovery and 1, 2, 3, 24 hours after transient spinal ischemia. After 24 hours, rats were euthenized and spinal cords were removed for the assay of DNA fragmentation. Other groups of rats received 5 minutes of ischemia, and after 1, 6, 24, 48 and 72 hours, spinal cords were removed for the assay of Bcl-2 family protein mRNA and DNA fragmentation. RESULTS: The neurologic injury and DNA fragmentation of sevoflurane group were significantly lesser than enflurane group. 5 minutes of IPC caused increase in Bcl-xl protein mRNA transcription at 48 and 72 hours reperfusion. There were no significant changes in neurologic injury, Bcl-2 family mRNA transcription and DNA fragmentation between control group, rapid group, and delayed group. CONCLUSIONS: Sevoflurane was effective in preventing neurologic injury after 13 minutes of transient spinal ischemia. However, rapid and delayed ischemic preconditioning did not potentiated neuroprotective action of sevoflurane during 15 minutes of spinal ischemia.

• Keywords: Bcl-2;DNA;Ischemic preconditioning;Neurologic;Sevoflurane;Spinal;