OPC-88117可抑制铯、4-氨基吡啶和洋地黄在犬浦肯野纤维及犬原位心脏中诱导产生的早期后去极化和延迟后去极化以及心律失常。

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.

作者信息

Graham B, Gilmour R F, Stanton M S, Zipes D P

机构信息

Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis.

出版信息

Am Heart J. 1989 Oct;118(4):708-16. doi: 10.1016/0002-8703(89)90583-8.

DOI:10.1016/0002-8703(89)90583-8

PMID:2552784

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 Vmax. 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.

摘要

新型抗心律失常药物OPC - 88117对早期后除极（EAD）和延迟后除极（分别为EAD和DAD）的影响在犬浦肯野纤维体外实验以及犬右心室体内实验中进行了评估。OPC - 88117具有与I类抗心律失常药物相似的电生理特性，即它降低了最大动作电位上升速率（Vmax）。OPC - 88117降低了由毒毛花苷诱导的DAD的幅度并延长了其耦联间期。同样，OPC - 88117抑制了4 - 氨基吡啶在体外诱导的EAD。在体内，OPC - 88117抑制了铯诱导的EAD、室性心律失常和房室传导阻滞。总之，OPC - 88117在体外抑制了DAD和EAD，并在犬原位心脏中抑制了EAD和触发活动。