To the Editor:—
The excellent article by Jonsson et al. 1provides biophysical insight into the mechanism of action of succinylcholine on the muscle-type acetylcholine receptors. They conclude that succinylcholine activates these receptors followed by desensitization.
The initial phase of activation results in an endplate potential that opens the adjacent voltage-gated sodium channel, resulting in repetitive waves of action potentials that manifest as initial muscle fasciculations. Because succinylcholine is not metabolized by the specific cholinesterase at the endplate, the succinylcholine-induced depolarization is maintained, and the outer voltage-gated sodium channel remains open. However, the inner time-dependent sodium gate will close, resulting in an endplate-muscular block. Because the depolarizing block is beyond the endplate, it is not characterized by tetanic fade or posttetanic facilitation and is potentiated by neostigmine (fig. 1A).
Prolonged exposure of the endplate to succinylcholine will result in progressive desensitization to the depolarizing action of succinylcholine, as well as to the chemical transmitter acetylcholine; hence, the block will gradually change from a depolarizing endplate-muscular block (Phase I) into a desensitizing Phase II neuromuscular block, which is characterized by progressive tetanic fade and posttetanic facilitation. The neuromuscular block may be antagonized by neostigmine. The degree of reversal by neostigmine is proportional to the extent of fade and posttetanic facilitation (fig. 1, B and C).2
American University of Beirut, Beirut, Lebanon. firstname.lastname@example.org