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The relation of plasma cholinesterases to response to clinical doses of succinylcholine

  • Werner Kalow
Article

Summary

The plasma cholinesterase of a normal adult is capable of destroyingin vitro up to 120 mg. per minute of succinylcholme chloride. This great speed of destruction cannot be obtainedin vivo, yet the normal plasma cholinesterase can effectively cope with a considerable excess of succmylcboline.

The rate of destruction of succinylcholine for any given concentration of succinylcholine is proportional to the concentration of plasma cholinesterase.

On slow intravenous infusion of succinyldichohne, the plasma cholinesterase must be assumed always to cause an accumulation of succinylmonochohne so that the concentration of succinylmonocholine exceeds by about 40 times the concentration of succinyldicholine. It is not yet clear whether this accumulation of succinylmonocholine is prevented by factors other than plasma cholinesterase, or whether this accumulation escapes clinical detection.

In order to exert its action at the neuromuscular junction, succinylcholine must enter the extravascular space where it is not exposed to plasma cholinesterase. Thus one cannot expect the esterase to be responsible for all abnormal reactions towards succinylcholine.

The sera of three patients are described, in these cholinesterase activity towards succinylcholine is too low to be measured. In all three cases the esterase has some peculiarities which are not fully explained. In one of these patients injection of 5 mg. of succinylcholine chloride was found to cause profound relaxation and 15 minutes’ apnoea.

Keywords

Cholinesterase Succinylcholine Succinyl Plasma Cholinesterase Single Muscle Fibre 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

La plasma cholinestérase d’un adulte normal peut détruirein vitro jusqu’à 120 mg. per minute de chlorure de suecinylcholine.in vitro, la réaction enzymatique n’est pas si rapide parce que la concentration plasmatique de la succinylcholine n’est pas assez élevée pour saturer l’enzyme. En d’autres mots, la plasma cholmestérase normale peut détruire plus de succinylcholine en peu de temps qu’il n’est nécessaire pour obtenir un effet de relâchement musculaire.

Pour une concentration donnée de succinylcholine, la vitesse de destruction doit être proportionnel au niveau plasmatique de la cholinestérase mêmesi l’estérase n’agit pas à sa capacité maximum.

Lorsqu’une solution de succinyldieholine est injectée lentement en intraveineuse, on doit toujours se rappeler que la plasma cholinestérase cause une accumulation de succinylmonocholine de sorte que la concentration de succinylmonocholine est environ 40 fois celle de la succinyldicholine. On ne connait pas encore si cette accumulation de succinylmonocholine est arrêtée par d’autres facteurs que la plasma cholmestérase ou bien si elle échappes à l’investigation clinique.

La succinylcholine agit à la jonction neuro-musculaire. Pour l’atteindre, la succinylcholine doit entrer dans le milieu extra cellulaire. Dans le liquide extravasculaire la succinylcholine n’est pas au contact de la plasma cholinestérase. En d’autres mots, l’estérase prévient l’entrée et la sorties dans les tissus mais ne peut être tenu responsable des irrégularités qui peuvent survenir dans les tissus au lieu d’action de la succinylcholine

Il est connu que la concentration de plasma cholinestérase varie d’une personne à une autre. Habituellement il s’agit et une variation de quantité de l’enzyme mais il peut survenir aussi des variations dans les propriétés de la plasma cholinestérase. Seulement dans trois de ces cas, l’activité de l’estérase sur la succinylcholine fût trop basse pour être mesurer. Chez l’un de ces patients, l’injection de 5 mg. de succinylcholine causa un relâchement musculaire profond et une apnée de 15 minutes.

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Copyright information

© Canadian Anesthesiologists 1956

Authors and Affiliations

  • Werner Kalow
    • 1
  1. 1.Department of PharmacologyUniversity of TorontoCanada

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