The beta 2-adrenergic agonist terbutaline suppresses acute passive transfer experimental autoimmune myasthenia gravis (EAMG).
Treatment of Lewis rats with the beta 2-adrenergic agonist terbutaline suppressed clinical symptoms of acute passive transfer EAMG induced with monoclonal anti-acetylcholine receptor antibody and accelerated clinical recovery in affected animals. Electrophysiological studies showed that the amplitude of the first compound muscle action potential was significantly larger in terbutaline-treated rats as compared to controls. In both groups, a comparable number of inflammatory cells at the muscle endplates was seen.
Chelmicka-Schorr
E
E
Department of Neurology, University of Chicago, IL 60637.
Wollmann
R L
RL
Kwasniewski
M N
MN
Kim
D H
DH
Dupont
B L
BL
D000208:Acute Disease; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D004576:Electromyography; D005260:Female; D007116:Immunization, Passive; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D009045:Motor Endplate / Q000276:immunology / Q000473:pathology; D009157:Myasthenia Gravis / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D011917:Rats, Inbred Lew; D013726:Terbutaline / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D007166:Immunosuppressive Agents; D013726:Terbutaline