BACKGROUND: Paraplegia is one of the most common complications following aortic aneurismal surgery. The present study examined the hypothesis that neuroprotection of sevoflurane postconditioning (PostC) against spinal cord reperfusion injury is associated with free radicals-mediated up-regulation of antioxidant enzymes in rabbits. MATERIALS AND METHODS: New Zealand White rabbits were subjected to sevoflurane PostC, oxygen (O(2)), or sham treatment at the onset of spinal cord reperfusion for 10 min. Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Forty-eight hours after reperfusion, the motor function of the lower limbs was evaluated and the lumbar spinal cord segment (L5-7) was harvested for histopathologic and biochemical analyses in the presence or absence of N-2-mercaptopropionylglycine, a potent oxygen free radical scavenger. RESULTS: Activities of superoxide dismutase and catalase in spinal cord tissue were increased in the sevoflurane PostC group 1 h after reperfusion and retained a higher level 6 or 24 h after reperfusion. Sevoflurane PostC produced a significant reduction of the malondialdehyde content at 6, 24, and 48 h after reperfusion. A 20 min continuous administration of N-2-mercaptopropionylglycine starting 10 min before the beginning of PostC attenuated the neuroprotective effect against spinal cord ischemia, and reversed the increase of the two enzyme activities in spinal cord tissue induced by sevoflurane PostC. CONCLUSION: An initial oxidative stress, as a trigger to up-regulate the antioxidant enzyme activities, plays an important role in the protection of sevoflurane PostC against spinal cord reperfusion injury.
BACKGROUND: Paraplegia is one of the most common complications following aortic aneurismal surgery. The present study examined the hypothesis that neuroprotection of sevoflurane postconditioning (PostC) against spinal cord reperfusion injury is associated with free radicals-mediated up-regulation of antioxidant enzymes in rabbits. MATERIALS AND METHODS: New Zealand White rabbits were subjected to sevoflurane PostC, oxygen (O(2)), or sham treatment at the onset of spinal cord reperfusion for 10 min. Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Forty-eight hours after reperfusion, the motor function of the lower limbs was evaluated and the lumbar spinal cord segment (L5-7) was harvested for histopathologic and biochemical analyses in the presence or absence of N-2-mercaptopropionylglycine, a potent oxygen free radical scavenger. RESULTS: Activities of superoxide dismutase and catalase in spinal cord tissue were increased in the sevoflurane PostC group 1 h after reperfusion and retained a higher level 6 or 24 h after reperfusion. Sevoflurane PostC produced a significant reduction of the malondialdehyde content at 6, 24, and 48 h after reperfusion. A 20 min continuous administration of N-2-mercaptopropionylglycine starting 10 min before the beginning of PostC attenuated the neuroprotective effect against spinal cord ischemia, and reversed the increase of the two enzyme activities in spinal cord tissue induced by sevoflurane PostC. CONCLUSION: An initial oxidative stress, as a trigger to up-regulate the antioxidant enzyme activities, plays an important role in the protection of sevoflurane PostC against spinal cord reperfusion injury.