BACKGROUND: Spinal cord ischemic injury occurring after surgical repair of thoracoabdominal aortic disease leaves a devastating complication. The purpose of this study was to evaluate the effects of anesthetic preconditioning on neurologic outcome and Bcl-2 family protein gene expression in transient spinal ischemia.

METHODS: In first experiment rats were divided by 4 groups and anesthetized with intraperitoneal propofol, enflurane, sevoflurane, or isoflurane. In second experiment, all rats were anesthetized with intraperitoneal propofol and enflurane, sevoflurane, isoflurane were given during 30 minutes and 14 minutes of spinal ischemia was induced 30 minutes later. Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. Neurologic scores were assessed 1, 3, 24, 48 hours after transient spinal ischemia. After 48 hours, rats were killed under anesthesia and spinal cords were removed for the assay of Bcl-2 family protein mRNA expression.

RESULTS: The neurologic injury of S and I group were significantly lesser than P group. 30 minutes of anesthetic preconditioning with enflurane, sevoflurane, and isoflurane showed significantly better neurologic outcome compared to propofol, enflurane, sevoflurane, or isoflurane anesthetized rats. Bcl-2 family protein mRNA expression of I group and IP group were lesser than the other groups.

CONCLUSIONS: Anesthetic preconditioning with volatile anesthetics for 30 minutes could reduce ischemic injury during transient spinal ischemia. The degree of neurologic injury may not be related to the expression of pro-apoptotic protein Bax. Isoflurane may have different influence on apoptosis after spinal ischemia compared to enflurane or sevoflurane.