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[麻醉诱导后丙胺卡因所致高铁血红蛋白血症增加]

[Increase of prilocaine-induced methemoglobinemia following anesthesia induction].

作者信息

Rudlof B, Durstewitz-Knierim D, Ridderskamp I, Scharenberg C, Brandt L

机构信息

Institut für Anästhesie der Kliniken der Stadt Wuppertal, Medizinische Fakultät der Universität Witten-Herdecke.

出版信息

Anaesthesist. 1995 Jun;44(6):445-9. doi: 10.1007/s001010050175.

Abstract

Although the local anaesthetic prilocaine is less cardio- and neurotoxic than lidocaine, it bears the disadvantage of the formation of methaemoglobin by the metabolite o-toluidine. Prilocaine is often successfully used, especially for the blockade of the brachial plexus, but one problem of this technique is the failure rate of 3-10%, with the consequence that general anaesthesia after administration of prilocaine is frequently necessary. Methaemoglobin formation after prilocaine administration has been thoroughly investigated. Nothing is known, however, about the interactions of prilocaine and the induction of general anaesthesia relative to methaemoglobinaemia. CASE REPORT. Two patients (47 and 52 years old) each received 500 mg prilocaine for the axillary blockade of the brachial plexus. After 100 and 120 min respectively, it was necessary to induce general anaesthesia, for which 350 mg thiopental, 1 mg alfentanil and 45 mg atracurium were used. At 15 min after induction, methaemoglobin levels had increased by 70% and 25%, respectively, from baseline before general anaesthesia. CONCLUSION. It is not possible to explain these findings conclusively with the present method. To check whether displacement of o-toluidine from the plasma protein binding might have been responsible, we provoked methaemoglobinaemia in vitro by adding o-toluidine to heparinised blood. Thiopental was then added to half the specimens. Subsequently, methaemoglobin levels were lower in the samples with thiopental. Three explanations seem plausible: (1) Thiopental blocks the hydroxylase of the endoplasmic reticulum, with the result that o-toluidine cannot be further metabolised, leading to higher o-toluidine and methaemoglobin levels. (2) Isoflurane improves the blood supply of the liver. This results in increased metabolism of prilocaine to o-toluidine. (3) The results were accidental. To clarify which of these explanations is correct, further investigation is necessary.

摘要

尽管局部麻醉药丙胺卡因的心脏毒性和神经毒性比利多卡因小,但其代谢产物邻甲苯胺会形成高铁血红蛋白,这是它的一个缺点。丙胺卡因经常被成功使用,尤其是用于臂丛神经阻滞,但该技术的一个问题是失败率为3% - 10%,结果是在使用丙胺卡因后经常需要进行全身麻醉。丙胺卡因给药后高铁血红蛋白的形成已经得到了充分研究。然而,关于丙胺卡因与全身麻醉诱导相对于高铁血红蛋白血症的相互作用却一无所知。病例报告。两名患者(分别为47岁和52岁)均接受了500毫克丙胺卡因用于臂丛神经的腋路阻滞。分别在100分钟和120分钟后,有必要诱导全身麻醉,为此使用了350毫克硫喷妥钠、1毫克阿芬太尼和45毫克阿曲库铵。诱导后15分钟时,高铁血红蛋白水平分别比全身麻醉前的基线水平升高了70%和25%。结论。用目前的方法无法确凿地解释这些发现。为了检查血浆蛋白结合中邻甲苯胺的置换是否可能是原因,我们通过向肝素化血液中添加邻甲苯胺在体外诱发高铁血红蛋白血症。然后向一半的样本中添加硫喷妥钠。随后,添加硫喷妥钠的样本中的高铁血红蛋白水平较低。三种解释似乎合理:(1)硫喷妥钠阻断内质网的羟化酶,结果邻甲苯胺无法进一步代谢,导致邻甲苯胺和高铁血红蛋白水平升高。(2)异氟烷改善肝脏的血液供应。这导致丙胺卡因向邻甲苯胺的代谢增加。(3)结果是偶然的。为了弄清楚这些解释中哪一个是正确的,有必要进行进一步的研究。

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