The effects of stylene maleinic acid butyl ester superoxide dismutase (SMA-SOD) on the brain damage induced by ischemia were studied in dogs. Eighteen minutes of cerebral ischemia was produced by clamping the ascending aorta with aorta-atrial and aorta-femoral vein bypass circuit. SMA-SOD(10mg/kg) was administered just after the initiation of recirculation. Dogs were divided into, control group and SMA-SOD group. In each group, cerebral blood flow (CBF) and intracranial pressure (ICP) were measured for 7 hours after ischemia, and neurologic outcome was evaluated up to 7 days after ischemia. Furthermore, extravasation of evans blue dye (EB, 100mg/kg) were observed 30 minutes after ischemia. SMA-SOD increased CBF during the hyperemia, and improved both delayed post-ischemic hypoperfusion (DHP) and neurologic outcomes. Extravasation of EB were recognized in the control group, but not in the SMA-SOD group.
In conclusion, vasogenic edema might play a role in the elevation of ICP besides the hyperemia, and SMA-SOD improved neurologic outcome by prevention of edema, and improvement of DHP. Furthermore, free radicals might play a role in the appearance of ischemic brain damage.