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Electrophysiology of Ethacizin: Effects on Arrhythmias in the In Situ Heart and Transmembrane Action Potentials of Purkinje Fibers and Ventricular Muscle Cells
Author(s) -
DANGMAN KENNETH H.,
ZAIM SINA,
HOFFMAN BRUCE N.,
HOFFMAN BRIAN F.
Publication year - 1990
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1990.tb01074.x
Subject(s) - purkinje fibers , medicine , cardiology , electrical conduction system of the heart , electrophysiology , qrs complex , anesthesia , electrocardiography
Therapeutic and Toxic Effects of Ethacizin . Ethacizin is a new antiarrhythmic drug that is a derivative of ethmozine. We confirmed the early findings that ethacizin reduces the arrhythmias that occur in dogs 24 hours after ligation of the left anterior descending coronary artery. However, we found that QRS duration and R‐on‐T beats were increased by ethacizin, and that sudden death occurred in one‐third of the dogs. In control experiments, etbmozine (n = 6) and quinidine (n = 6) produced antiarrhythmic effects comparable to those of ethacizin, but sudden death did not occur. Studies then were carried out on canine cardiac tissues using standard microelectrode techniques. Ethacizin 300 ng/mL decreased dV/dt max in Purkinje fibers and ventricular muscle. These decreases were rate dependent. Ethacizin decreased action potential plateau duration (APD‐60 mV) in false tendon Purkinje fibers, and increased it in ventricular muscle. In spontaneously firing Purkinje fibers, ethacizin consistently decreased high‐potential (normal) and low‐potential (abnormal) automaticity to 14% and 12% of control, respectively. The effects of ethacizin on catecholamine‐enhanced high‐potential automaticity were more variable. Automaticity decreased in about half of the fibers, but did not change greatly in the remainder. The antiarrhythmic actions of ethacizin may result from reduction of impulse initiation or conduction in Purkinje fibers or myocardial cells. ( J Cardiovasc Electrophysiol, Vol. 1, pp. 411–425, October 1990 )