E ect of methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on lipid peroxidation (LP) was evaluated in an experimental model of spinal cord compression injury in anesthetized rats. Forty rats, divided randomly into four groups, were injured by compressing on the spinal cord at Th 3 for 1 min. Bolus injections of saline solution, MP (30 mg/kg bolus and 5.4 mg/kg/h), TM (10 mg/kg four times per day), or vitamin E (30 mg/ kg four times per day) were begun 1 h after the spinal cord injury (SCI). Twenty-four hours after treatment, the rats were killed, and malondialdehyde (MDA), a LP product, was measured in the spinal cord tissues. Rats treated with MP, TM and vitamin E had signi®cantly decreased MDA levels (P50.01) than rats in the control group. The lowest MDA levels were found in the TM group. These results suggest that MP, TM and vitamin E may have a protective e ect against SCI in rats by its antioxidant e ect.
Trauma-induced lipid peroxidation (LP) is one of the most important factors that produces tissue damage in head trauma. In the present study, the protective effects of free radical suppression with methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on the development of cerebral LP and oedema resulting from head trauma have been investigated. Rats were divided randomly into four groups. Bolus injections of physiological saline, MP (initial 30 mg/kg for 1 h, continuing administration of 5.4 mg/kg per hour until 24 h), TM (10 mg/kg), or vitamin E (30 mg/kg) were given 1 h after the head trauma. The animals were killed 24 h after the weight-drop injury for removal of the brain, and the malondialdehyde (MDA) level and water content of the brain were determined. Rats treated with TM had MDA levels which decreased significantly in comparison with the control group (P<0.03), and none of the drugs had an effect on LP and water content of the brain (P>0.05) that was statistically different. These findings demonstrated the beneficial effect of TM in this model of experimental brain injury.
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