Hay D W, Wadsworth R M
Eur J Pharmacol. 1982 Feb 5;77(4):221-8. doi: 10.1016/0014-2999(82)90122-4.
Local anaesthetic activity was measured on the rat phrenic nerve at 37 degrees C: Verapamil HCl had 5.1X and methoxyverapamil HCl had 3.0X the potency of lidocaine. Flunarizine was about equipotent with lidocaine, while nifedipine, diazoxide and sodium nitroprusside were without effect. It is concluded tht the smooth muscle inhibitory actions of the calcium antagonists, even when used in concentrations possessing local anaesthetic activity, are due to a reduction in Ca2+ permeability. In rat isolated vasa deferentia, lidocaine had both stimulant and inhibitory actions. On its own it induced rhythmic contractions (not blocked by phentolamine) and it also augmented the frequency of rhythmic contractions produced by methoxamine or barium. These actions may be due to block of K+ channels. Lidocaine also reduced the amplitude of methoxamine and barium induced contractions and both phases of the KCl contraction. The KCl response was restored by increasing "Ca2+]0, and it is therefore concluded that lidocaine was acting by blockade of Ca2+ channels.
在37摄氏度下对大鼠膈神经测量局部麻醉活性：盐酸维拉帕米的效力是利多卡因的5.1倍，盐酸甲氧维拉帕米是利多卡因的3.0倍。氟桂利嗪与利多卡因效力大致相当，而硝苯地平、二氮嗪和硝普钠则无作用。得出结论，钙拮抗剂的平滑肌抑制作用，即使在使用具有局部麻醉活性的浓度时，也是由于Ca2+通透性降低所致。在大鼠离体输精管中，利多卡因具有刺激和抑制作用。它自身可诱导节律性收缩（不受酚妥拉明阻断），还可增加甲氧明或钡产生的节律性收缩频率。这些作用可能是由于K+通道的阻断。利多卡因还降低了甲氧明和钡诱导的收缩幅度以及氯化钾收缩的两个阶段。通过增加[Ca2+]0可恢复氯化钾反应，因此得出结论，利多卡因是通过阻断Ca2+通道起作用的。
