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目的研究异丙酚对交感神经元全细胞钠通道电流的影响，探讨其外周血管扩张机制。方法酶消化法急性分离ＳＤ大鼠（８～１２ｄ）颈上交感神经节细胞，应用全细胞膜片钳技术记录异丙酚对钠通道电流的影响。结果在钳制电压（Ｖｈ）－８０ｍＶ，刺激电压（Ｖｔ）０ｍＶ条件下，临床相关浓度的异丙酚（５．６μｍｏｌ／Ｌ）使钠通道电流峰值降２７．６６％（Ｐ＜０．０１），随浓度增加，抑制作用逐渐增强（ｒ＝０．９８２，Ｐ＜０．０１），５０％的钠通道电流峰值受抑制时的异丙酚浓度（ＩＣ５０）约为 ３２．１９μｍｏｌ／Ｌ；５６μｍｏｌ／Ｌ的异丙酚使钠电流稳态失活曲线产生明显的超极化方向移动（１８．５４ｍＶ，Ｐ＜０．０１），用药前、后 ５０％的通道失活时的条件脉冲电压（Ｖ１／２）分别为：－４０．０２ｍＶ、－５８．５６ｍＶ；５６μｍｏｌ／Ｌ的异丙酚使钠电流的激活曲线产生轻微的去极化方向移动（ ４． ４９ｍＶ， Ｐ＜ ０． ０５）。结论临床相关浓度的异丙酚对交感神经节全细胞钠通道电流有明显的抑制作用，且呈浓度依赖性；其抑制作用主要与钠通道的失活有关。提示异丙酚的循环抑制作用可能与其直接抑制交感神经有关。
Objective To investigate the effect of propofol on the sodium channel current of sympathetic neurons and explore the mechanism of peripheral vasodilation. Methods The cervical sympathetic ganglion cells were isolated from SD rats (8 ~ 12 days) by enzymatic digestion. The effects of propofol on sodium channel current were recorded by whole-cell patch-clamp technique. Results The clinically relevant concentration of propofol (5.6 μmol / L) decreased the peak current of sodium channel by 27.66% (P <0.01) at clamping voltage (Vh) -80mV and stimulating voltage (Vt) (R = 0.982, P <0.01). The concentration of propofol (IC50) at the peak of 50% sodium channel inhibition was about 32.19μmol / L and the concentration of 56μmol Propofol / L produced a significant hyperpolarization shift (18.54mV, P <0.01) in the steady-state inactivation curve of sodium current, and the condition impulse voltage V1 / 2) were: -40.02mV, -58.56mV; 56μmol / L of propofol sodium current activation curve generated a slight depolarization direction of movement (4.49mV, P <0.05). Conclusions Propofol at a clinically relevant concentration significantly inhibits sodium current in sympathetic ganglion cells in a concentration-dependent manner, and its inhibitory effect is mainly related to inactivation of sodium channels. Tip propofol cycle inhibition may be directly related to its inhibition of sympathetic.