title: Exacerbated muscle dysfunction by procainamide in rats with experimental myasthenia gravis.
abstract: 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.
authors.affiliation: Department of Microbiology, University of Texas Health Science Center, San Antonio 78284.
authors.forename: T M
authors.initials: TM
authors.lastname: Yeh
authors.forename: J A
authors.initials: JA
authors.lastname: Tami
authors.forename: K A
authors.initials: KA
authors.lastname: Krolick
mesh_terms: D000818:Animals; D000906:Antibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000503:physiopathology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D009119:Muscle Contraction / Q000187:drug effects*; D009157:Myasthenia Gravis / Q000503:physiopathology*; D011342:Procainamide / Q000633:toxicity*; D051381:Rats; D011917:Rats, Inbred Lew; D011950:Receptors, Cholinergic / Q000276:immunology / Q000378:metabolism
chemical_list: D000906:Antibodies; D011950:Receptors, Cholinergic; D011342:Procainamide