Abstract
Purpose
Mivacurium is metabolized by plasma cholinesterase catalyzed ester hydrolysis. Acetylcholinesterase antagonists used in the reversal of muscle relaxation may also inhibit plasma cholinesterase and, therefore, delay the hydrolysis of mivacurium. The clinical interaction between acetylcholinesterase antagonists and mivacurium induced neuromuscular blockade was studied.
Method
Intraoperative muscle relaxation was maintained with a mivacurium infusion to achieve a constant intense block (first twitch, T1, 2–3% of control). Patients were randomly divided into three groups. Patients in Group 1 received no anticholinesterase, in Group 2 neostigmine 0.07 mg · kg−1, and in Group 3 edrophonium 1 mg · kg−1. The times between termination of the mivacurium infusion (Group 1) or the administration of the anticholinesterase (Groups 2 and 3) to 25%, 50%, 75% and 95% T1 recovery, and to 50%, 70% and 90% recovery in the ratio, T4/T1 (TR) were recorded.
Result
In the neostigmine Group, T1 recovery to 25%, 50% and 75% ( 2.32 ± 1.41, 3.90 ± 1.85 and 6.88 ± 2.66 min) was accelerated compared with control (3.36 ± 1.34, 5.78 ± 2.22, and 8.58 ± 3.60, and), but recovery to 95% (18.53 ± 9.09 vs 13.29 ± 5.24 min) was delayed. Also, TR recovery to 50%, 70%, and 90% was slower (14.47 ± 8.73, 21.25 ± 11.06 and 31.37 ± 12.11 min vs 11.75 ± 3.74, 13.78 ± 4.39 and 17.86 ± 6.44 min). However, all T1 and TR recovery times were decreased in the edrophonium group (0.88 ± 0.51, 2.00 ± 1.50, 4.97 ± 2.96, and 9.35 ± 5.24 min for T1 and 6.86 ± 3.93, 9.05 ± 4.51 and 12.24 ± 6.66 min for TR).
Conclusion
Neostigmine reversal of intense mivacurium neuromuscular block should be avoided, as this may result in prolongation of the block.
Résumé
Objectif
Le mivacurium est hydrolysé par un ester catalysé pr la cholinestérase plasmatique. Les antagonistes de l’acetylcholinestérase utilisés pour inverser la relaxation musculaire peuvent aussi inhiber la cholinestérase plasmatique et, par conséquent, retarder l’hydrolyse du mivacurium. Cette étude portait sur l’interaction clinique entre les antagonistes de l’acétylcholinestérase et le bloc neuromusculaire induit par le mivacurium.
Méthodes
La relaxation musculaire peropératoire était maintenue par une perfusion de mivacurium pour procurer une curarisation profonde et continue (premier twitch, T1 à 2–3% du contrôle). Les patients étaient répartis aléatoirement entre trois groupes. Les patients du groupe 1 ne recevaient pas d’anticholinestérase, le groupe 2, de la néostigmine 0,07 mg-kg−1 et le groupe 3, de l’édrophonium 1 mg · kg−1. Les intervalles entre l’arrêt de la perfusion de mivacurium (groupe 1) ou entre l’administration de l’anticholinestérase (groupes 2 et 3) et la récupération à 25%, 50%, 75% et 95% de T1, et la récupération à 50%, 70% et 90% du rapport T4/T1 (TR) étaient enregistrés.
Résultats
Dans le groupe néostigmine, la récupération de T1 à 25%, 50% et 75% (2,32 ± 1,41, 3,90 ± 1,85 et 6,88 ± 2,66 min) était accélérée comparativement au contrôle (3,36 ± 1,34, 5,78 ± 2,22 et 8,58 ± 3,60) mais la récupération à 95% (18,53 ± 9,09 vs 13,29 ± 5,24 min) était retardée. De plus, la récupération de TR à 50%, 70% et 95% se faisait plus lentement (14,47 ± 8,73, 21,25 ± 11,05 et 31,27 ± 12,11 min vs 11,75 ± 3,74, 13,78 ± 4,39 et 17,86 ± 6,4 min). Cependant, tous les intervalles de récupération à T1 et de TR étaient diminués dans les groupes édrophonium (0,88 ± 0,52, 2,00 ± 1,50, 4,97 ± 2,96 et 9,35 ± 5,25 min pour T1 et 6,86 ± 3,93, 9,05 ± 4,51 et 12,24 ± 6,66 min pour TR).
Conclusion
L’inversion par le néostigmine du bloc neuromusculaire profond au mivacurium devrait être évitée, parce qu ’il est possible qu ’elle prolonge le bloc.
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This work was performed at University of California Irvine Medical Center, Orange, California.
Supported by an education grant from Burroughs Wellcome Co.
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Kao, Y.J., Le, N.D. The reversal of profound mivacurium-induced neuromuscular blockade. Can J Anaesth 43, 1128–1133 (1996). https://doi.org/10.1007/BF03011839
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DOI: https://doi.org/10.1007/BF03011839