Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury

Objective: Primary impact to the spinal cord causes rapid oxidative stress after injury. To protect neural tissue, it is important to prevent secondary pathophysiological mechanisms. Etomidate, a strong antiexcitotoxic agent, stimulates the gamma aminobutyric acid (GABA) receptors. The purpose of this study was to investigate neurobehavioral and histological recovery and to evaluate the biochemical responses to treatment of experimental spinal cord injury (SCI) in rats with etomidate or methylprednisolone (MP) or both etomidate and MP. Material and methods: Seventy-two rats were randomly allocated into six groups: a control group (laminectomy alone), a trauma group (laminectomy + trauma), a methylprednisolone group (30 mg/kg MP), an etomidate group (2 mg/kg), a methylprednisolone, and etomidate combined treatment group (30 mg/kg MP and 2 mg/kg etomidate) and a vehicle group. Six rats from each group were killed at the 24th hour after the injury. Malondialdehyde, glutathione, nitric oxide and xanthine oxidase levels were measured. Neurological functions of the remaining rats were recorded weekly. Six weeks after injury, all of those rats were killed for histopathological assesssment. Conclusion: Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MR In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection. (c) 2006 ISDN. Published by Elsevier Ltd. All rights reserved.