1995 Volume 44 Issue 1 Pages 1-8
Multiple factors alter the interaction of muscle relaxants with the neuromuscular (NM) junction. This review focused on the aberrant responses caused, principally, by alterations in acetylcholine receptor (AChR)s. It should be emphasized that prejunctional and post AChR factors also may alter sensitivity to muscle relaxants and also cause functional changes, including muscle weakness. The pharmacokinetic and pharmacogenetic factors which cause aberrant responses have not been discussed. Many pathological states increase or decrease AChRs and this has been enumerated in Table 1. Increased AChRs is associated with resistance to the NM effects of nondepolarizing (ND)MR. With proliferation of AChR, the exaggerated release of potassium with depolarization from succinylcholine (SCh) can be attributed to increased AChR number; qualitative changes in AChR number may also play a role. Preliminary studies using potassium channel inhibitors indicate that potassium channels do not play a major role in the hyperkalimic response to SCh. During acute organophosphorus poisoning, SCh should be avoided because its metabolic breakdown would be impared;1 the requirement for NDMR may be increased because of increased competition with high leels of ACh at the neuromuscular junction. With the chronic presence of ACh at the neuromuscular junction there would be down regulation and the responses would be similar to that seen in myasthenia gravis. All of these responses to SCh and NDMR which are associated with concomitant changes in AChR are analogus to drug-receptor interactions observed in other biological systems.