title: Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.affiliation: Inonu University, School of Medicine, Department of Neurosurgery, Turgut Ozal Medical Center, 44069 Malatya, Turkey.
authors.forename: Suleyman R
authors.initials: SR
authors.lastname: Cayli
authors.forename: Ozkan
authors.initials: O
authors.lastname: Ates
authors.forename: Nese
authors.initials: N
authors.lastname: Karadag
authors.forename: Eyup
authors.initials: E
authors.lastname: Altinoz
authors.forename: Neslihan
authors.initials: N
authors.lastname: Yucel
authors.forename: Saim
authors.initials: S
authors.lastname: Yologlu
authors.forename: Ayhan
authors.initials: A
authors.lastname: Kocak
authors.forename: Celal Ozbek
authors.initials: CO
authors.lastname: Cakir
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D005045:Etomidate / Q000627:therapeutic use*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007796:Laminectomy / Q000379:methods; D008315:Malondialdehyde / Q000378:metabolism; D008775:Methylprednisolone / Q000627:therapeutic use; D009043:Motor Activity / Q000187:drug effects; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D020127:Recovery of Function / Q000187:drug effects*; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism; D018709:Statistics, Nonparametric; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D018696:Neuroprotective Agents; D009569:Nitric Oxide; D008315:Malondialdehyde; D014969:Xanthine Oxidase; D005978:Glutathione; D008775:Methylprednisolone; D005045:Etomidate