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去极化和非去极化神经肌肉阻滞剂引起的张口阻力变化。

Changes in resistance to mouth opening induced by depolarizing and non-depolarizing neuromuscular relaxants.

作者信息

van der Spek A F, Reynolds P I, Fang W B, Ashton-Miller J A, Stohler C S, Schork M A

机构信息

Department of Anesthesiology, University of Michigan, Ann Arbor 48109.

出版信息

Br J Anaesth. 1990 Jan;64(1):21-7. doi: 10.1093/bja/64.1.21.

Abstract

Mouth opening was measured in 43 children anaesthetized with isoflurane and paralysed with vecuronium or suxamethonium. Measurements of mouth opening were made for up to 10 min after loss of the adductor pollicis twitch and cessation of muscle fasciculations. In 22 patients receiving suxamethonium, a significant (P less than 0.001) reduction in mean mouth opening occurred in the 60 s after loss of twitch and cessation of fasciculations. Mouth opening reductions could last for up to 10 min after the loss of twitch, beyond the return of the twitch. One patient experienced "masseter spasm"; he did not develop malignant hyperpyrexia during 2.5 h of isoflurane anaesthesia. Patients receiving vecuronium showed a significant (P less than 0.0006) increase in mouth opening. In 20 subjects, mouth opening was generated with a small (1.67 N) and a larger (4.32 N) force. Proportionally equal reductions in mouth opening were obtained with either force after suxamethonium administration. Relatively equal increases with either force followed vecuronium administration. Isolated masseter spasm is not pathognomonic for malignant hyperpyrexia. If the diagnosis of malignant hyperpyrexia is contemplated, signs of hypermetabolism, such as increases in end-tidal carbon dioxide concentration during constant minute ventilation, should be sought.

摘要

对43例接受异氟烷麻醉并用维库溴铵或琥珀胆碱使其麻痹的儿童进行了张口度测量。在内收拇指肌颤搐消失和肌肉束颤停止后长达10分钟内进行张口度测量。在22例接受琥珀胆碱的患者中,在颤搐消失和束颤停止后的60秒内,平均张口度出现了显著(P<0.001)降低。张口度降低在颤搐消失后可持续长达10分钟,超过颤搐恢复时间。1例患者出现“咬肌痉挛”;在2.5小时的异氟烷麻醉期间未发生恶性高热。接受维库溴铵的患者张口度出现了显著(P<0.0006)增加。在20名受试者中,分别用小(1.67N)和大(4.32N)的力量产生张口动作。给予琥珀胆碱后,两种力量产生的张口度降低比例相等。给予维库溴铵后,两种力量产生的张口度增加相对相等。孤立的咬肌痉挛并非恶性高热的特征性表现。如果考虑诊断恶性高热,应寻找高代谢的迹象,如在恒定分钟通气量时呼气末二氧化碳浓度升高。

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