Subarachnoid hemorrhage increases superoxide dismutase activity in canine cerebral arteries

The mechanisms underlying the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH) are not well understood. Previous studies demonstrated that the cerebral arterial wall is exposed to oxidative stress after SAH. The superoxide anion (O₂^-) appears to be an important mediator of vasospasm. The present study was designed to characterize superoxide dismutase (SOD) activity in cerebral arteries obtained from normal dogs as well as from dogs exposed to SAH. The "double hemorrhage" canine model of the disease was used. Large cerebral arteries were dissected and superoxide dismutase activity was assayed spectrophotometrically by the inhibition of the reduction of acetylated cytochrome C in a xanthine/xanthine oxidase system. Seven days after SAH, we found significant increase (P < 0.05) in total vascular SOD activity in arteries exposed to autologous blood. Normal middle cerebral artery SOD activity was 40 ± 4 vs. 65 ± 9 U/mg protein in SAH. Total SOD activity in the circle of Willis was 42 ± 4 vs. 56 ± 4, normal vs. SAH. Similarly SOD activity in the posterior cerebral artery was 41 ± 1 vs. 49 ± 3, normal vs. SAH. Our results suggest that SAH may increase the activity of SOD in cerebral arteries. The detected increase in SOD activity may represent adaptive response of the vascular wall to the oxidative stress after SAH.