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Propofol decreases the axonal excitability in rat primary sensory afferents

机译:丙泊酚降低大鼠原发性感觉传入神经轴突兴奋性

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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 (0 μMol: 0.96 ± 0.07 ms; 1000 μMol 1.10 ± 0.06 ms, P < 0.01). Also, propofol prolonged the relative refractory period (0 μMol: 1.79 ± 1.13 ms; 100 μMol: 2.53 ± 1.38 ms, P < 0.01), and reduced superexcitability (0 μMol: - 14.0 ± 4.0%; 100 μMol: - 9.5 ± 5.5%) and subexcitability (0 μMol: 7.5 ± 1.2%; 1000 μMol: 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.
机译:目的:本研究的目的是研究丙泊酚产生的周围感觉神经兴奋性的变化。主要方法:在最近描述的啮齿类动物大隐神经的体外模型中,我们使用阈值跟踪(QTRAC?)技术来测量由异丙酚引起的Aβ纤维轴突神经兴奋性的变化。测试了10μMol,100μMol和1000μMol的浓度。记录潜伏期,峰值响应,强度持续时间常数(τSD)和感觉神经元动作电位(SNAP)的恢复周期。关键发现:我们的结果表明,异丙酚在体外会降低大鼠原发性感觉传入神经的神经兴奋性。延迟随浓度增加而增加(0μMol:0.96±0.07 ms; 1000μMol1.10±0.06 ms,P <0.01)。此外,丙泊酚延长了相对不应期(0μMol:1.79±1.13 ms; 100μMol:2.53±1.38 ms,P <0.01),并且降低了超兴奋性(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)在恢复周期中显着(P <0.01)。意义:我们的研究结果表明,异丙酚会降低初级感觉传入神经的神经兴奋性。阈值跟踪技术揭示了轴突电压门控离子通道受丙泊酚的影响很大,因此可能至少部分负责较早描述的镇痛作用。

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