The major advance from which we are beginning to reap the benefits is the development of analytical techniques to measure muscle relaxant or antagonist concentrations in blood and body tissues. We now can define the alterations that disease and physiological changes make in the rate at which the relaxant leaves the plasm (pharmacokinetics), and in the sensitivity of the neuromuscular junction to muscle relaxants (pharmacodynamics). This information will allow a more selective approach to relaxant dose and help us to avoid the wide variability previously described.⁴ The search for a short-acting non-depolarizing muscle relaxant is not yet over. In the antagonist area, 4-aminopyridine has advantages over neostigmine and pyridostigmine in that concomitant atropine administration is not required and antibiotic-induced neuromuscular blocks are more consistently antagonized. Because 4-aminopyridine may have potentially undesirable side-effects, smaller doses in combination with neostigmine may be advantageous. Lastly, several factors which may augment a non-depolarizing neuromuscular blockade and/ or interfere with antagonism are reviewed. If neostigmine 2.5 to 3.0 mg/70 kg, or pyridostigmine 10 to 15 mg/kg does not antagonize the block, those factors should be considered before additional antagonist is given.

De nombreux auteurs, dont Katz, ont souligné la variabilité de la réponse des malades aux relaxants musculaires; cette variabilité n’est pas intrinsèque aux drogues elles-mêmes mais peut partiellement s’expliquer; ainsi, la pharma-cocinétique cherche à identifier les facteurs qui modifient le taux de ľélimination plasmatique du relaxant musculaire et de son côté, la pharmacodynamie cherche à identifier les causes de la modification de la sensibilité de la plaque neurale aux relaxants musculaires. Quand on aura réponse à ces interrogations, on saura utiliser les myorésolutifs en contournant cette variabilité.