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异丙酚降低大鼠初级感觉传入纤维的轴突兴奋性。

Propofol decreases the axonal excitability in rat primary sensory afferents.

机构信息

Institute of Anesthesiology, University Hospital of Zurich, Switzerland.

出版信息

Life Sci. 2012 Feb 27;90(9-10):343-50. doi: 10.1016/j.lfs.2011.12.007. Epub 2011 Dec 28.

DOI:10.1016/j.lfs.2011.12.007
PMID:22227474
Abstract

AIMS

The aim of this present study was to investigate the changes of peripheral sensory nerve excitability produced by propofol.

MAIN METHODS

In a recently described in vitro model of rodent saphenous nerve we used the technique of threshold tracking (QTRAC®) to measure changes of axonal nerve excitability of Aβ-fibres caused by propofol. Concentrations of 10 μMol, 100 μMol and 1000 μMol were tested. Latency, peak response, strength-duration time constant (τSD) and recovery cycle of the sensory neuronal action potential (SNAP) were recorded.

KEY FINDINGS

Our results have shown that propofol decreases nerve excitability of rat primary sensory afferents in vitro. Latency increased with increasing concentrations (0μMol: 0.96 ± 0.07ms; 1000μMol 1.10 ± 0.06ms, P<0.01). Also, propofol prolonged the relative refractory period (0μMol: 1.79 ± 1.13ms; 100 μMol: 2.53 ± 1.38ms, P<0.01), and reduced superexcitability (0 μMol: -14.0±4.0%; 100μMol: -9.5 ± 5.5%) and subexcitability (0μMol: 7.5 ± 1.2%; 1000μMol: 3.6 ± 1.2) significantly during the recovery cycle (P<0.01).

SIGNIFICANCE

Our results have shown that propofol decreases nerve excitability of primary sensory afferents. The technique of threshold tracking revealed that axonal voltage-gated ion channels are significantly affected by propofol and therefore might be at least partially responsible for earlier described analgesic effects.

摘要

目的

本研究旨在探讨丙泊酚对周围感觉神经兴奋性的影响。

方法

在最近描述的鼠隐神经体外模型中,我们使用阈跟踪(QTRAC®)技术来测量丙泊酚引起的 Aβ纤维轴突神经兴奋性的变化。测试了 10μMol、100μMol 和 1000μMol 三种浓度。记录潜伏期、峰值反应、强度-持续时间时间常数(τSD)和感觉神经元动作电位(SNAP)的恢复周期。

主要发现

我们的结果表明,丙泊酚降低了体外大鼠初级感觉传入纤维的神经兴奋性。潜伏期随浓度增加而增加(0μMol:0.96±0.07ms;1000μMol:1.10±0.06ms,P<0.01)。此外,丙泊酚延长了相对不应期(0μMol:1.79±1.13ms;100μMol:2.53±1.38ms,P<0.01),并显著降低了超兴奋性(0μMol:-14.0±4.0%;100μMol:-9.5±5.5%)和亚兴奋性(0μMol:7.5±1.2%;1000μMol:3.6±1.2%)在恢复周期中(P<0.01)。

意义

我们的结果表明,丙泊酚降低了初级感觉传入纤维的神经兴奋性。阈跟踪技术表明,轴突电压门控离子通道明显受丙泊酚影响,因此至少部分负责早期描述的镇痛作用。

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