Fink B R
Anesthesiology. 1982 Sep;57(3):167-71. doi: 10.1097/00000542-198209000-00004.
The interaction of glucose lack and local anesthetic on impulse conduction was investigated in rabbit vagus nerve. Glucose lack depressed the compound action potential 50 per cent in 47 +/- 7 min (+/- SD, n = 5) and extinguished it in 69 +/- 7 min. Lidocaine hydrochloride, 0.1 mmol/1 (0.0027 g/dl), delayed the onset of inexcitability caused by glucose lack: 50 per cent depression required 85 +/- 9 min, extinction required 131 +/- 20 min (P less than 0.001). The delay decreased with lower and higher lidocaine concentrations. Lidocaine also significantly decreased the potassium loss and sodium gain occasioned by 2.5 h of glucose deprivation. Thus, delayed extinction of excitability by local anesthetic in very low concentration may be due to decrease in permeability of the axonal plasma membrane not only to sodium but also to potassium ions.
在兔迷走神经中研究了葡萄糖缺乏与局部麻醉药对冲动传导的相互作用。葡萄糖缺乏在47±7分钟（±标准差，n = 5）内使复合动作电位降低50%，并在69±7分钟内使其消失。0.1 mmol/1（0.0027 g/dl）的盐酸利多卡因延迟了由葡萄糖缺乏引起的兴奋性丧失的开始：50%的降低需要85±9分钟，消失需要131±20分钟（P<0.001）。随着利多卡因浓度的降低和升高，延迟时间缩短。利多卡因还显著减少了2.5小时葡萄糖剥夺所引起的钾流失和钠增加。因此，极低浓度的局部麻醉药延迟兴奋性消失可能是由于轴突质膜对钠和钾离子的通透性降低所致。
