Neuroprotective effect of epidural electrical stimulation against ischemic spinal cord injury in rats - Electrical preconditioning

Neuroprotective effect of epidural electrical stimulation against ischemic spinal cord injury in rats - Electrical preconditioning
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DOI:
10.1097/00000542-200507000-00015
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发表时间:
2005-07-01
期刊:
影响因子:
8.8
通讯作者:
Sugahara, K
Sugahara, K
中科院分区:
医学1区
文献类型:
--
作者:
Kakinohana, M;Harada, H;Sugahara, K

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背景:电休克疗法可能作为诱导缺血性脑损伤耐受的有效预处理刺激。目前的研究探讨是否对脊髓的电刺激也能够诱导耐受缺血性脊髓损伤的短暂性aortic occlusion.Methods:脊髓缺血引起的胸降主动脉闭塞,结合保持全身低血压(40毫米汞柱)在该过程中。植入硬膜外电极的动物根据电刺激和假手术分为四组。两组均于脊髓缺血前30 min行快速预处理(RE组,n = 8)和假手术(RC组,n = 8)。延迟预处理组(DE组,n = 8)和假手术组(DC组,n = 8)分别于预处理后24 h阻断主动脉9 min。另外,在硬膜外电刺激或假刺激后30 min或24 h,将大鼠暴露于脊髓缺血6-11 min。P50组代表脊髓缺血的持续时间与50%的概率导致paraplegation.Results:预处理与电刺激DE组,而不是RE组保护脊髓免受缺血,这种刺激延长P50在DE组与DC组相比约15.0%。虽然这种电预处理的最佳设置应在未来的研究中确定,但结果表明,硬膜外电刺激将是一种有用的方法来提供脊髓缺血保护。
Background: Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion.Methods: Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia.Results: Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group.Conclusions: Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will he a useful approach to provide spinal protection against ischemia.