Preferential block of small myelinated sensory and motor fibers by lidocaine -: In vivo electrophysiology in the rat sciatic nerve

Preferential block of small myelinated sensory and motor fibers by lidocaine -: In vivo electrophysiology in the rat sciatic nerve
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DOI:
10.1097/00000542-200112000-00025
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发表时间:
2001-12-01
期刊:
影响因子:
8.8
通讯作者:
Strichartz, GR
Strichartz, GR
中科院分区:
医学1区
文献类型:
--
作者:
Gokin, AP;Philip, B;Strichartz, GR

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背景神经纤维对局麻药的敏感性差异及其与选择性功能障碍的关系仍存在争议。在目前的研究中,我们报告了经皮注射利多卡因后大鼠坐骨神经纤维的传导阻滞的特点,这与临床应用非常相似。(体重,300-400 g)在全身麻醉期间,记录不同类别的感觉轴突的冲动(大的,A α和β纤维;小的,A δ有髓纤维和无髓C纤维)和运动轴突(大的,A α纤维;小的,A γ有髓纤维)。刺激坐骨神经远端,并记录从L4-L5背根(感觉)和腹根(运动)引出的小细丝的冲动,这些小细丝从脊髓中急性切开。将浓度为0.05-1%的利多卡因以0.1-ml的溶液经皮注射到坐骨切迹处。利多卡因对强直性(0.5 Hz刺激)和使用依赖性(A δ和A γ纤维40 Hz刺激,C纤维5 Hz刺激)的冲动抑制进行了测定。最小有效(阈值)利多卡因浓度(即,阻断10%的纤维传导),对于感觉,A δ为0.03%,A α β为0.07%,C纤维为0.09-0.1%,对于运动,A γ为0.03%,A α纤维为0.05%。纤维敏感性的顺序,根据产生50%的峰值紧张性纤维阻滞(IC 50)的浓度排序,是A γ> A δ = A α> A α β> C。传导速度快的C纤维(传导速度> 1 m/s)比传导速度慢的C纤维(传导速度< 1 m/s; IC 50 = 0.30%)更敏感(IC 50 = 0.13%)。在1%利多卡因时,所有纤维均被强直性阻滞。依赖于利多卡因的影响只占一个温和的增强块(在利多卡因浓度为0.25%)在A δ和A γ纤维,在C纤维相位刺激有更小的影响,有时缓解紧张block.Conclusions:敏感性利多卡因并不严格遵循“大小原则”,较小(较慢)轴突总是首先被阻止。这种纤维阻滞的顺序与先前报道的经皮利多卡因后大鼠功能缺陷的顺序定性一致,即运动=本体感受>伤害感受。如果我们假设运动缺陷首先由A γ纤维的传导失败引起,而伤害感受依赖于C纤维传导。
Background Controversy still surrounds the differential susceptibility of nerve fibers to local anesthetics and its relation to selective functional deficits. In the current study we report features of conduction blockade in different classes of rat sciatic nerve fibers after injection of lidocaine by a percutaneous procedure that closely resembles clinical applications.Methods: In 30 adult male Sprague-Dawley rats (weight, 300-400 g) during general anesthesia, impulses were recorded in different classes of sensory axons (large, A alpha and beta fibers; small, A delta myelinated fibers and unmyelinated C fibers) and motor axons (large, A alpha fibers; small, A gamma myelinated fibers) classified by conduction velocity. The sciatic nerve was stimulated distally, and impulses were recorded from small filaments teased from L4-L5 dorsal (sensory) and ventral (motor) roots sectioned acutely from the spinal cord. Lidocaine at concentration of 0.05-1% was injected percutaneously in 0.1-ml solutions at the sciatic notch. Both tonic (stimulated at 0.5 Hz) and use-dependent (stimulated at 40 Hz for A delta and A gamma fibers and at 5 Hz for C fibers) impulse inhibitions by lidocaine were assayed.Results. Minimal effective (threshold) lidocaine concentrations (i.e., to block conduction in 10% of fibers) were, for sensory, 0.03% for A delta, 0.07% for A alpha beta, and 0.09-0.1% for C fibers, and for motor, 0.03% for A gamma and 0.05% for A alpha fibers. The order of fiber susceptibility, ranked by concentrations that gave peak tonic fiber blockade of 50% (IC50s), was A gamma > A delta = A alpha > A alpha beta > C. Faster-conducting C fibers (conduction velocity > 1 m/s) were more susceptible (IC50 = 0.13%) than slower ones (conduction velocity < 1 m/s; IC50 = 0.30%). At 1% lidocaine, all fibers were tonically blocked. Use-dependent effects accounted for only a modest potentiation of block (at a lidocaine concentration of 0.25%) in A delta and A gamma fibers, and in C fibers phasic stimulation had even smaller effects and sometimes relieved tonic block.Conclusions: Susceptibility to lidocaine does not strictly follow the "size principle" that smaller (slower) axons are always blocked first. This order of fiber blockade is qualitatively consistent with previous reports of the order of functional deficits in the rat after percutaneous lidocaine, that is, motor = proprioception > nociception, If we assume that motor deficits first arise from conduction failure in A gamma fibers and that nociception relies on C fiber conduction.