摘要
外周神经损伤常可诱发神经支配区行为上的痛觉过敏和感觉异常,神经损伤区传递冲动的能力丧失和引起神经髓鞘膜的脱落。从损伤神经纤维上可记录到来源于损伤区的异常传入电活动,K^+通道阻断剂四乙酸乙酸盐(TEA)诱发脱髓鞘膜区产生异常传入电活动。而山莨菪碱(Anisodamini)则可消除来自损伤区的异常电活动。这种病理动物经过WS-频谱仪发出的远红外线连续2周(总计24小时)的照射后。痛觉过敏消失,原来被阻断的神经动作电位的传导功能部分恢复,TEA诱发出的异常电活动减弱或消失;同时山莨菪碱对记录到的自发放电的影响减弱。提示远红外线的照射对损伤外周神经异常功能活动的抑制以及部分功能的恢复可能与通过恢复神经轴索膜的结构有关。
A peripheral nerve injury with demyelination was produced in adult rats by placing loosely constrictive ligatures around the sciatic nerve. The postoperative behaviour of these rats indicated abnormabilities like those seen in man, such as hyperalgesia, allodynia and conductive interruption of the nerve in the operated hindlimb, at the same time, spontaneous ectopic afferent discharges originated from the damaged region were recorded and showed facilitation by TEA, and blockade by anisodamine locally or systemically used. After the operated hindlimb in this neuropathic model accepted a series of far-infrared irradiation generated from WS-frequence apparatus, the result demonstrated that not only the hyperalgesia of behavious disappeared and the conduction of the nerve partly recovered, but also no responses to both TEA and anisodamine were present. A possible mechanism of physiotherapeutic effect was discussed.
出处
《基础医学与临床》
CSCD
1991年第6期350-354,共5页
Basic and Clinical Medicine
关键词
外周神经损伤
远红外线
照射
demyelination hyperalegsia anisodamine physiotherapy ectopic discharges
