OPC-88117 suppresses early and delayed afterdepolarizations and arrhythmias induced by cesium, 4-aminopyridine and digitalis in canine Purkinje fibers and in the canine heart in situ

Brett Graham, Robert F. Gilmour, Marshall S. Stanton, Douglas P. Zipes

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

The effects of OPC-88117, a new investigational antiarrhythmic drug, on early and delayed afterdepolarizations (EAD and DAD, respectively) were assessed in vitro in canine Purkinje fibers and in vivo in the canine right ventricle. OPC-88117 had similar electrophysiologic properties to class I antiarrhythmic agents in that it decreased V̇max. OPC-88117 decreased the amplitude and prolonged the coupling interval of DAD induced by acetylstrophanthidin. Likewise, OPC-88117 suppressed EAD induced in vitro by 4-aminopyridine. In vivo, cesium-induced EAD, ventricular arrhythmia, and atrioventricular block were suppressed by OPC-88117. In summary, OPC-88117 suppressed DAD and EAD in vitro and inhibited EAD and triggered activity in the in situ canine heart.

Original languageEnglish (US)
Pages (from-to)708-716
Number of pages9
JournalAmerican Heart Journal
Volume118
Issue number4
DOIs
StatePublished - Oct 1989

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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