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琥珀酰胆碱:肌束震颤的机制以及d -筒箭毒碱或苯妥英对其的预防作用。

Succinylcholine: mechanism of fasciculations and their prevention by d-tubocurarine or diphenylhydantoin.

作者信息

Hartman G S, Fiamengo S A, Riker W F

出版信息

Anesthesiology. 1986 Oct;65(4):405-13. doi: 10.1097/00000542-198610000-00010.

DOI:10.1097/00000542-198610000-00010
PMID:3767039
Abstract

Administration of d-tubocurarine (dTC) or diphenylhydantoin (DPH) was evaluated as a pretreatment to prevent succinylcholine (Sch) evoked fasciculations. Experiments were designed to determine the nature of the drug-drug interactions, sites of interaction, and site of fasciculation suppression. Sch is known to evoke repetitive discharge generation by motor nerve terminals (MNTs). Transmission of these prejunctional discharges causes fasciculations. A cat soleus neuromuscular preparation in situ, which enables recording of nerve action potentials initiated by MNTs, their transmitted muscle action potentials, and the resultant contractile responses, was used to explore Sch effects before and after iv pretreatment with dTC or DPH. dTC is known to act prejunctionally to suppress repetitive discharges initiated by facilitatory drugs and tetanic conditioning of MNTs. Accordingly, pretreatment with dTC 50 micrograms X kg-1 suppressed the Sch-induced MNT repetitive discharging and correspondingly suppressed generalized fasciculations without affecting twitch. This dTC dose, however, also reduced Sch blocking potency by 33%, slowed its rate, and shortened block duration. These latter effects represent competitive postjunctional antagonism. DPH is also known to suppress MNT repetitive discharging. Correspondingly, Sch-induced repetitive firing and ensuing fasciculations were suppressed by DPH (30 mg X kg-1) without affecting twitch. Unlike dTC, this DPH dose increased Sch blocking potency by 50%, increased the initial rate of block, and did not alter block duration. These DPH effects were dose-dependent and within the anticonvulsant range for cats. Therefore, patients with anticonvulsant levels of DPH may not require pretreatment before Sch.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

评估了给予d -筒箭毒碱(dTC)或苯妥英(DPH)作为预处理以预防琥珀酰胆碱(Sch)诱发的肌束颤动。实验旨在确定药物 - 药物相互作用的性质、相互作用位点以及肌束颤动抑制位点。已知Sch可通过运动神经末梢(MNTs)诱发重复放电。这些节前放电的传递会导致肌束颤动。使用原位猫比目鱼肌神经肌肉标本,该标本能够记录由MNTs引发的神经动作电位、其传递的肌肉动作电位以及由此产生的收缩反应,以探究静脉注射dTC或DPH预处理前后Sch的作用。已知dTC在节前起作用,抑制由易化药物引发的重复放电以及MNTs的强直条件作用。因此,用50微克/千克的dTC预处理可抑制Sch诱导的MNT重复放电,并相应地抑制全身性肌束颤动,而不影响抽搐。然而,该dTC剂量也使Sch的阻滞效能降低了33%,减缓了其起效速度,并缩短了阻滞持续时间。后一种效应代表竞争性节后拮抗作用。已知DPH也可抑制MNT重复放电。相应地,DPH(30毫克/千克)可抑制Sch诱导的重复放电及随之而来的肌束颤动,而不影响抽搐。与dTC不同,该DPH剂量使Sch的阻滞效能提高了50%,增加了初始阻滞速度,且未改变阻滞持续时间。这些DPH效应呈剂量依赖性,且在猫的抗惊厥范围内。因此,DPH处于抗惊厥水平的患者在使用Sch之前可能无需预处理。(摘要截断于250字)

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