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硬膜外灌注冷却对兔脊髓缺血具有保护作用。胆碱能功能评估。

Epidural perfusion cooling protects against spinal cord ischemia in rabbits. An evaluation of cholinergic function.

作者信息

Malatová Z, Vanický I, Gálik J, Marsala M

机构信息

Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovak Republic.

出版信息

Mol Chem Neuropathol. 1995 Jun-Aug;25(2-3):81-96. doi: 10.1007/BF02960903.

Abstract

The protective effect of regional epidural spinal cord cooling was evaluated in a rabbit spinal cord ischemia model. Hypothermia was performed by the continual perfusion of 2-4 degrees C cold saline in the epidural space around the ischemic lumbar segments, 4 min before and during ischemia. The spinal cord was deeply hypothermic (21 degrees C) throughout the whole ischemic period. Ischemia was induced by the occlusion of the abdominal aorta for 40 min under normothermic or hypothermic conditions. Recovery of motor and sensory functions, spinal cord-evoked potentials, and motor-evoked potentials were then evaluated up to 24 h postischemia. After this period, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were measured, in particular, zones of the lumbar spinal cord. AChE was also investigated histochemically. Animals in the normothermic group displayed fully developed spastic paraplegia with near complete loss of spinal somatosensory and motor-evoked potentials. AChE histochemistry showed extensive necrotic changes affecting lumbosacral gray matter. These changes corresponding with the pronounced losses of ChAT and AChE activities indicated irreversible injury of the spinal cord. In contrast, after hypothermic ischemia, animals survived without any sign of neurological impairment with almost full recovery of the spinal cord-evoked potentials. ChAT and AChE activities in the gray matter showed near control values corresponding with histochemical analysis of fully preserved gray matter. Hypothermia under the present experimental conditions efficiently protected the spinal cord against ischemic injury.

摘要

在兔脊髓缺血模型中评估了局部硬膜外脊髓降温的保护作用。在缺血前4分钟及缺血期间,通过在缺血腰段周围的硬膜外间隙持续灌注2-4℃冷盐水来进行低温处理。在整个缺血期间,脊髓处于深度低温状态(21℃)。在常温或低温条件下,通过阻断腹主动脉40分钟诱导缺血。然后在缺血后24小时内评估运动和感觉功能、脊髓诱发电位和运动诱发电位的恢复情况。在此期间过后,测量胆碱乙酰转移酶(ChAT)和乙酰胆碱酯酶(AChE)的活性,特别是腰段脊髓的区域。还对AChE进行了组织化学研究。常温组的动物表现出完全发展的痉挛性截瘫,脊髓体感和运动诱发电位几乎完全丧失。AChE组织化学显示腰骶部灰质有广泛的坏死变化。这些与ChAT和AChE活性明显丧失相对应的变化表明脊髓发生了不可逆损伤。相比之下,低温缺血后,动物存活且没有任何神经功能障碍的迹象,脊髓诱发电位几乎完全恢复。灰质中的ChAT和AChE活性显示接近对照值,这与完全保留的灰质的组织化学分析结果相符。在本实验条件下,低温有效地保护脊髓免受缺血性损伤。

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