Kennett R P, Gilliatt R W
University Department of Clinical Neurology, Queen Square, London, England.
Muscle Nerve. 1991 Jun;14(6):553-62. doi: 10.1002/mus.880140610.
In rabbits, the tibial nerve was exposed in the lower thigh under general anesthesia and cooled in a metal trough at 1 to 2 degrees C or 5 degrees C for 2, 3, or 4 hours. Nerve conduction studies showed local failure of conduction at the site of cooling which persisted after rewarming, and which was followed by distal degeneration of affected fibers. No persistent conduction block was seen. Changes in maximal velocity indicated that the fastest-conducting motor and afferent axons had been preferentially affected. Histological findings in nerves examined at different intervals after cooling confirmed the physiological evidence of primary axonal damage, affecting particularly large diameter fibers. Paranodal demyelination was inconspicuous and restricted to regions just proximal to sites of axonal degeneration. No segmental demyelination was seen. These results clarify previous uncertainties as to the time-course and distribution of nerve damage after local cooling at temperatures just above freezing point.
在兔身上，在全身麻醉下暴露大腿下部的胫神经，并在金属槽中于1至2摄氏度或5摄氏度冷却2、3或4小时。神经传导研究显示，冷却部位出现局部传导障碍，复温后仍持续存在，随后受影响纤维发生远端变性。未见持续性传导阻滞。最大速度的变化表明，传导速度最快的运动和传入轴突受到了优先影响。冷却后不同时间检查神经的组织学结果证实了原发性轴突损伤的生理学证据，尤其影响大直径纤维。结旁脱髓鞘不明显，仅限于轴突变性部位近端的区域。未见节段性脱髓鞘。这些结果澄清了之前关于在略高于冰点的温度下局部冷却后神经损伤的时间进程和分布的不确定性。
