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 assessment. RESULTS: Etomidate treatment revealed similar neurobehavioral and histopathological recovery to MP treatment 6 weeks after injury. Combined treatment did not provide additional neuroprotection. CONCLUSION: Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MP. In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection.
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 assessment. RESULTS:Etomidate treatment revealed similar neurobehavioral and histopathological recovery to MP treatment 6 weeks after injury. Combined treatment did not provide additional neuroprotection. CONCLUSION:Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MP. In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection.
Authors: Mário Sérgio Lima de Lavor; Nancy Scardua Binda; Fabíola Bono Fukushima; Fátima Maria Caetano Caldeira; Juliana Figueira da Silva; Carla Maria Osório Silva; Karen Maciel de Oliveira; Bernardo de Caro Martins; Bruno Benetti Junta Torres; Isabel Rodrigues Rosado; Renato Santiago Gomez; Marcus Vinícius Gomez; Eliane Gonçalves de Melo Journal: Int J Clin Exp Pathol Date: 2015-09-01
Authors: Adem Aslan; Mustafa Cemek; Mehmet Emin Buyukokuroglu; Korhan Altunbas; Orhan Bas; Yusuf Yurumez; Murat Cosar Journal: Eur Spine J Date: 2009-05-26 Impact factor: 3.134