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针对实验性缺血性脊髓损伤的保护作用。

Protection against experimental ischemic spinal cord injury.

作者信息

Robertson C S, Foltz R, Grossman R G, Goodman J C

出版信息

J Neurosurg. 1986 Apr;64(4):633-42. doi: 10.3171/jns.1986.64.4.0633.

Abstract

The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.

摘要

作者研究了通过用阻断神经元活动并直接或间接降低组织代谢的药物预处理来保护兔脊髓免受缺血损伤。在缺血前,采用低温、硫喷妥钠、镁、利多卡因和纳洛酮对脊髓进行预处理。低温和硫喷妥钠提供了相当的保护作用:它们各自将使50%的动物产生神经功能缺损所需的缺血持续时间从26分钟增加到41分钟。它们还将脊髓体感诱发电位(SSEP)的突触后波消失但动物仍有神经功能恢复的时间从10分钟增加到30分钟。低温和硫喷妥钠联合使用时,使50%的动物产生神经功能缺损所需的缺血持续时间增加到57分钟。纳洛酮使50%的动物产生神经功能缺损所需的缺血持续时间增加到36分钟,并将SSEP的突触后波消失但动物仍有神经功能恢复的时间增加到20分钟。镁预处理改善了神经功能结局,可能是通过改善侧支循环,因为并非所有动物在主动脉阻断期间SSEP都完全消失。利多卡因没有益处,可能是由于导致的低血压持续时间延长。

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