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Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a reversible arterial narrowing occurring as a result of the mechanical and physiologic effects of blood products. Multiple factors are effective in the development of arterial narrowing; they provide long-term arterial contraction, inhibition of vasodilatation, and depression of the metabolic, immunoreactive, and inflammatory processes. We assessed Na selenite, which activates calpain II and promotes intracellular Ca2+ influx, by increasing oxygen radical synthesis in SAH. We also assessed amiloride, which involves non–voltage-graded Na channels, Na+/Ca2+ exchange, and Na+/H+ antiport mechanism and antioxidative effects. We evaluated the morphologic and biochemical effects of Na selenite and amiloride on basilar arterial smooth muscle vessels in SAH.Twenty pigs were randomly allocated to 4 groups. In group 1 only SAH was created. In group 2, after SAH, subcutaneously amiloride was applied once a day for 4 weeks. In group 3, after SAH subcutaneous Na selenite was applied once a day for 4 weeks. In group 4, after SAH, amiloride and Na+ selenite were given subsequently once a day for 4 weeks. The effects of amiloride and Na selenite on the ATPase and malondialdehyde (MDA) levels, and on Superoxide dismutase activity (SOD), and the resulting histopathologic findings were studied.In group 2, the vessel SOD level was 3 times higher than in group 1, but the Na+ K+ ATPase and MDA levels were found to be similar. In group 3, SOD activity was found to be similar to that in group 1. but Na+ K+ ATPase and MDA levels were 3 times higher than group 1. In group 4, SOD activity was very high in comparison with groups 3 and 1, whereas MDA level was half that found in group 3. ATPase levels did not show a significant difference from those in group 2.These results demonstrate that amiloride is not effective in basilar arterial changes due to SAH. However, amiloride protects the side effects of Na+ selenite. We suggest that this protection occurs by blocking the effect of Na+ selenite on oxidation and on the Ca2+ influx mechanism.