Actions and clinical assessment of drugs which produce neuromuscular block / W.D.M. Paton and Eleanor J. Zaimis.

  • Paton, William D. M.
Date:
[1950?]
Catalogue details

Licence: In copyright

Credit: Actions and clinical assessment of drugs which produce neuromuscular block / W.D.M. Paton and Eleanor J. Zaimis. Source: Wellcome Collection.

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    blocking effect on tibialis from 60% to 75% block and prolongs it. (3) But these changes of potency of decamethonium and d-tubocurarine do not affect different muscles equally or in the same direction. Fig. 1 shows, for instance, that with the soleus muscle adrenaline has quite opposite effects to those on tibialis ; here it actually augments the action of decamethonium. With d-tubocurarine, however, adrenaline hardly modifies the action on soleus and increases it on tibialis (fig. 2). The presence of circulating adrenaline, therefore, has three effects : (1) it increases the stimulant action of decamethonium ; (2) it changes the potency of d-tubo- curarine and of decamethonium on a given muscle; and (3) it changes the pattern of muscle susceptibility to these two drugs in opposite ways, increasing the proportionate effect of decamethonium on the “ red ” muscle, soleus, and decreasing that of d-tubocurarine on soleus. There can be little doubt that tests of these compounds in conscious people will be seriously influenced by the secretion of adrenaline that accompanies trials of this nature. Idiosyncrasy Among the precautions taken in the administration of d-tubocurarine is that of giving an initial small dose, so as to detect those occasional persons who are particu¬ larly susceptible to it, and who (it has been suggested) may be regarded as latent or subclinical myasthenics. The same technique has been used with decamethonium (Gray 1950). But when we consider the modes of action of the two drugs, and the evidence already cited that conditions favouring the action of d-tubocurarine usually oppose that of decamethonium, it seems reasonable to expect that those patients who are susceptible to d-tubocurarine would be, if anything, resistant to decamethonium. Some slight support for this suggestion that there is no idiosyncrasy of this kind to decametho¬ nium comes from the experience of Davies (1950) in which, out of 973 administrations of decamethonium, every patient required 3-5 mg., and none appeared to be particularly sensitive. It would be of great interest to know what the sensitivity of a myasthenic is to decamethonium, since it would not only determine whether idiosyncrasy of this kind occurred to deca¬ methonium but would also throw light on the pathogenesis of myasthenia. It therefore seems probable that precautionary small initial doses are unnecessary with decamethonium. They may also be somewhat confusing to an inexperienced anaesthetist. The effects of a small dose of decamethonium in a conscious patient with (no doubt) a liberal supply of circulating adrenaline due to the approaching operation