Cayli Suleyman R, Ates Ozkan, Karadag Nese, Altinoz Eyup, Yucel Neslihan, Yologlu Saim, Kocak Ayhan, Cakir Celal Ozbek
Inonu University, School of Medicine, Department of Neurosurgery, Turgut Ozal Medical Center, 44069 Malatya, Turkey.
Int J Dev Neurosci. 2006 Jun;24(4):233-9. doi: 10.1016/j.ijdevneu.2006.04.003. Epub 2006 May 15.
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.
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.
Etomidate treatment revealed similar neurobehavioral and histopathological recovery to MP treatment 6 weeks after injury. Combined treatment did not provide additional neuroprotection.
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.
脊髓受到的原发性损伤会在损伤后迅速引发氧化应激。为保护神经组织，预防继发性病理生理机制至关重要。依托咪酯是一种强效抗兴奋毒性剂，可刺激γ-氨基丁酸（GABA）受体。本研究的目的是调查大鼠实验性脊髓损伤（SCI）经依托咪酯或甲泼尼龙（MP）或依托咪酯与MP联合治疗后的神经行为和组织学恢复情况，并评估其生化反应。
72只大鼠被随机分为六组：对照组（仅行椎板切除术）、创伤组（椎板切除术+创伤）、甲泼尼龙组（30mg/kg MP）、依托咪酯组（2mg/kg）、甲泼尼龙与依托咪酯联合治疗组（30mg/kg MP和2mg/kg依托咪酯）以及溶媒组。每组6只大鼠在损伤后24小时处死，测量丙二醛、谷胱甘肽、一氧化氮和黄嘌呤氧化酶水平。其余大鼠每周记录神经功能。损伤6周后，所有大鼠处死进行组织病理学评估。
依托咪酯治疗在损伤6周后显示出与MP治疗相似的神经行为和组织病理学恢复。联合治疗未提供额外的神经保护作用。
脊髓损伤后立即进行依托咪酯治疗具有与MP相似的神经保护作用。尽管神经保护机制不同，但MP与依托咪酯联合治疗并未提供额外的保护。
