Kalichman M W, Powell H C, Reisner L S, Myers R R
J Neuropathol Exp Neurol. 1986 Sep;45(5):566-75. doi: 10.1097/00005072-198609000-00006.
In order to evaluate the possible mechanisms of local anesthetic toxicity, the rat sciatic nerve was exposed to various solutions including Nesacaine (containing the antioxidant sodium bisulfite), 2-chloroprocaine in the Nesacaine vehicle (0.2% sodium chloride), 0.2% sodium bisulfite in 0.2% sodium chloride, or 0.2% sodium chloride alone. All solutions were pH balanced between 2.9 and 3.2. Forty-eight hours (h) following extraneural administration of 1 ml volumes, significant edema was produced by all solutions containing 3% 2-chloroprocaine, but not with 0.2% bisulfite in sodium chloride or with sodium chloride alone. Intrafascicular administration of five to ten microliter volumes of these solutions produced edema at 48 h in all cases, but the highest levels were observed with Nesacaine and the lowest levels with 0.2% bisulfite. The results of this study implicate the local anesthetic 2-chloroprocaine in the production of nerve edema, which is inconsistent with other reports that the toxicity of Nesacaine-CE can be attributed to the antioxidant bisulfite.
为了评估局部麻醉药毒性的可能机制，将大鼠坐骨神经暴露于各种溶液中，包括奴佛卡因（含抗氧化剂亚硫酸氢钠）、在奴佛卡因溶媒（0.2%氯化钠）中的2-氯普鲁卡因、0.2%氯化钠中的0.2%亚硫酸氢钠或仅0.2%氯化钠。所有溶液的pH值均平衡在2.9至3.2之间。在神经外给予1毫升体积的溶液48小时后，所有含3% 2-氯普鲁卡因的溶液均产生了明显的水肿，但0.2%亚硫酸氢钠溶液或仅氯化钠溶液未产生水肿。在所有情况下，将这些溶液5至10微升体积束内给药48小时均产生了水肿，但奴佛卡因组水肿程度最高，0.2%亚硫酸氢钠组最低。本研究结果表明，局部麻醉药2-氯普鲁卡因与神经水肿的产生有关，这与其他报道认为奴佛卡因CE的毒性可归因于抗氧化剂亚硫酸氢钠的观点不一致。
