Exacerbated muscle dysfunction by procainamide in rats with experimental myasthenia gravis

The induction of experimental autoimmune myasthenia gravis (EAMG) has long been shown to result in inefficient function of the acetylcholine receptor (AChR) and concomitant impairment of AChR-dependent neuromuscular communication. As an animal model of human myasthenia gravis, AChR-immunized rats demonstrate symptoms of MG very similar to those observed in human patients resulting from the presence of circulating anti-AChR antibodies which interfere with the normal function of the receptor. In addition to antibody antagonists of neuromuscular function, a variety of drugs have been observed to be associated with possible exacerbations of impaired neuromuscular function leading to myasthenic crisis in some MG patients. One drug, the cardiac anti-arrhythmic agent, procainamide, has been reported to cause both pre-synaptic and post-synaptic electrophysiologic effects at the neuromuscular junction. The study described below extends these observations to include the demonstration of perturbed AChR-dependent contractile muscle function in a rat model of MG.