Effects of Nimodipine and Magnesium Sulfate on Endogenous Antioxidant Levels in Brain Tissue After Experimental Head Trauma *Mehmet Erkan Üstün, **Ates ¸ Duman, **Cemile Öztin Ög ˘ün, †Hüsamettin Vatansev, and ‡Ahmet Ak Departments of *Neurosurgery, **Anesthesiology and Intensive Care, †Biochemistry, and ‡Emergency, Selçuk University, Faculty of Medicine, Konya, Turkey Summary: To examine the effects of calcium antagonists nimodipine and magnesium sulfate (MgSO 4 ) on tissue endogenous antioxidant levels, the authors studied superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels in rabbit brain 1 hour after experimental head trauma. Forty New Zealand rabbits were anesthetized and randomly divided into four groups. Group 1 (n  10) was the sham operated group. Group 2 (n  10), the control group, received head trauma and no treatment. Group 3 (n  10) received head trauma and intravenous (IV) 2 gr/kg nimodipine. Group 4 (n  10) received head trauma and IV 100 mg/kg MgSO 4 . Head trauma was delivered by per- forming a craniectomy over the right hemisphere and dropping a weight of 20 g from a height of 40 cm. In the right (traumatized) hemisphere, SOD and GPx decreased by 57.60% ± 9.60% and 72.93% ± 5.51% respectively from sham values. Magnesium sulfate, but not nimodipine, reduced the magnitude of decrease of SOD and GPx to 19.43% ± 7.15% and 39.01% ± 7.92% respectively from sham values. In the left (non- traumatized) hemisphere, MgSO 4 increased SOD to 42.43% ± 24.76% above sham values. The authors conclude that MgSO 4 treatment inhibited the decrease in SOD and GPx levels in experimental brain injury. Key Words: Glutathione peroxidase—Head trauma—Magnesium sulfate—Nimodipine-Rabbit—Superoxide dismutase Much work has been done on the mechanisms of brain injury after ischemia and trauma. Decreases in cellular energy stores cripple ion-pumping mechanisms that main- tain very low concentrations of calcium (Ca ++ ) and so- dium (Na + ) inside the cell (1). Intracellular calcium cata- lyzes the conversion of xanthine dehydrogenase to xanthine oxidase, which produces superoxide from mito- chondria (1,2). Moreover, superoxide generation is postu- lated to further elevate intracellular calcium (3). Superox- ide, either directly or after conversion to hydroxyl radical, damages biologic membranes and other cellular compo- nents including DNA, resulting in cell death (4–6). In low pH, superoxide is converted to perhydroxyl radical. When perhydroxyl radical reacts with superoxide, it forms hy- drogen peroxide (7,8). Superoxide dismutase (SOD) con- verts superoxide to oxygen and hydrogen peroxide. Glu- tathione peroxidase (GPx) converts hydrogen peroxide to water and oxidized glutathione (GSSG) (8,9,10). Nimodipine is a voltage activated calcium-channel blocker active in the brain. By blocking calcium channels in neurones and cerebral blood vessels it should reduce intracellular calcium concentrations after ischemic or trau- matic injury, and thus secondarily decrease free radical production (1,11). Magnesium sulfate (MgSO 4 ) is a natu- Address correspondence and reprint requests to Dr. Cemile Öztin Ög ˘ün, Selçuk Üniversitesi T1p Fakültesi, Anestezi ve Reanimasyon Anabilimdal1, Akyokus ¸, 42,080 Konya, Turkey. Journal of Neurosurgical Anesthesiology Vol. 13, No. 3, pp. 227–232 © 2001 Lippincott Williams & Wilkins, Inc., Philadelphia 227