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Canadian Journal of Anesthesia, Vol 46, 1156-1163, Copyright © 1999 by Canadian Anesthesiologists' Society
ARTICLES |
S Sano, S Yokono, H Kinoshita, K Ogli, H Satake, T Kageyama and S Kaneshina
Department of Anesthesiology and Emergency Medicine, Kagawa Medical University, Japan. sanosyu@yahoo.co.jp
PURPOSE: To measure the dynamic penetration process of lidocaine, lidocaine concentration (Ci) and pH (pHi) in squid giant axon, and to determine the times and Ci of disappearance and reappearance of action potentials (AP). METHODS: Lidocaine solutions adjusted to four different pHs (pH = 5.5, 6.8, 7.8 and 9.0) were externally administered to the axon and Ci and pHi were measured using lidocaine and pH microsensors. The times and Ci when the AP just disappeared and reappeared were recorded. In addition, for comparison with Ci, the lidocaine content in the whole axon (Cw) was measured with high-performance liquid chromatography (HPLC). RESULTS: The Ci (charged plus uncharged) was 1.5 times greater than the uncharged form of administered lidocaine. The changes in pHi depended on the increase in Ci. The AP disappeared only after administration of high pH lidocaine solutions (pH = 7.8, 9.0) and reappeared by washing out the solution in the chamber. Nerve block occurred more rapidly at pH 9.0 than at pH 7.8, and the time after washing out the lidocaine was longer at pH 9.0 than at pH 7.8. The mean Ci and charged lidocaine concentration in the axoplasm, when the AP disappeared or reappeared, were lower at pH 9.0 than at pH 7.8 (P < 0.05). CONCLUSION: Uncharged lidocaine penetrates the axon membrane to the axoplasm where it changes to the charged form and is concentrated in the axon membrane and axoplasm. External application of uncharged lidocaine plays a role in modulating nerve conduction.
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