Exacerbated muscle dysfunction by procainamide in rats with experimental myasthenia gravis

Trai Ming Yeh, Joseph A. Tami, Keith A. Krolick

Research output: Contribution to journalArticle

1 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)53-65
Number of pages13
JournalDrug and Chemical Toxicology
Volume15
Issue number1
DOIs
StatePublished - Jan 1 1992

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis
  • Chemical Health and Safety

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