Abstract

Although use of corticosteroid in the management of head trauma has caused a great deal of controversy, corticosteroids have long been an adjunct in the management of severe closed head injury. The glucocorticoid steroid methylprednisolone (MP) has been proven to have significant antioxidant effect when administered in an antioxidant-high dose after central nervous system injury. The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K(+)/Mg(+2) ATPase EC.3.6.1.3.) activity, lipid peroxidation, and early ultrastructural findings were determined during the immediate posttraumatic period in rats. Mechanical brain injury was produced when a calibrated weight-drop device is allowed to fall on the skull's convexity over the right hemisphere, 1 to 2 mm lateral from the midline. In group I, rats were used to determine Na(+)-K(+)/Mg(+2) ATPase activity, the extent of lipid peroxidation, by measuring the level of malondialdehyde content and normal ultrastructural findings in two different brain areas (cerebral cortex and brain stem). In group II, physiologic saline was administered right after trauma in the same amount as methylprednisolone. In group III rats, methylprednisolone (30 mg/kg) was administered intravenously right after trauma. Na(+)-K(+)/Mg(+2) ATPase activity significantly decreased in the cerebral cortex and in brain stem within 2 hours after trauma (p < 0.05). There was significant difference in malondialdehyde content between groups II and III (p < 0.05). Methylprednisolone treatment reduced malondialdehyde content and induced the recovery of Na(+)-K(+)/Mg(+2) activity. These data suggest that inactivation of Na(+)-K(+)/Mg(+2) ATPase is closely correlated to changes of lipid peroxidation and the alteration of the ultrastructural findings in the early phases after head trauma. The glucocorticoid steroid methylprednisolone has been proven to have significant effect in activation of Na(+)-K(+)/Mg(+2) ATPase with significant reduction of malondialdehyde content.

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