Lowndes H E, Pagès B, Bessou P
Eur J Pharmacol. 1979 Jan 1;53(2):159-66. doi: 10.1016/0014-2999(79)90161-4.
The effects of lidocaine (1--20 microgram/ml) on afferent discharge patterns of primary endings of muscle spindles in cat tenuissimus muscle were investigated. Discharge from the endings, recorded in Ia afferent axons, was evoked by ramp stretch of the muscle, stimulation of single static or dynamic fusimotor axons or by a combination of stretch and fusimotor stimulation. Spontaneous discharge of the endings at the initial length of the muscles was reduced by 2--5 microgram/ml and abolished by 10--15 microgram/ml lidocaine. The static but not the dynamic discharge elicited by muscle stretch was blocked by concentrations of 10--15 microgram/ml. The same concentrations abolished static and dynamic fusimotor influences on primary ending discharge. However, in one experiment where the spindle was microscopically observed, fusimotor stimulation still resulted in contraction of the intrafusal muscle even when fusimotor stimulation failed to elicit changes in discharge response patterns of the primary endings. These findings indicate that lidocaine interferes with the encoding mechanism prior to block of impulse conduction in either the fusimotor or afferent axons.
研究了利多卡因（1 - 20微克/毫升）对猫薄肌肌梭初级终末传入放电模式的影响。记录在Ia类传入轴突中的终末放电，通过肌肉的斜坡拉伸、单根静态或动态梭内肌运动轴突的刺激或拉伸与梭内肌运动刺激的组合来诱发。肌肉初始长度时终末的自发放电在利多卡因浓度为2 - 5微克/毫升时减少，在10 - 15微克/毫升时消失。肌肉拉伸引起的静态而非动态放电在浓度为10 - 15微克/毫升时被阻断。相同浓度消除了静态和动态梭内肌运动对初级终末放电的影响。然而，在一个对肌梭进行显微镜观察的实验中，即使梭内肌运动刺激未能引起初级终末放电反应模式的变化，梭内肌运动刺激仍导致梭内肌收缩。这些发现表明，利多卡因在阻断梭内肌运动或传入轴突中的冲动传导之前，就干扰了编码机制。
