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Alterations to the electrical activity of atrial muscle isolated from the rat heart, produced by exposure in vitro to amiodarone
Author(s) -
Northover B.J.
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb16458.x
Subject(s) - amiodarone , stimulation , chemistry , medicine , membrane potential , electrophysiology , cardiac muscle , in vitro , sodium channel , endocrinology , sodium , antiarrhythmic agent , pharmacology , biochemistry , atrial fibrillation , organic chemistry , heart disease
1 Glass microelectrodes were used to record transmembrane electrical activity from cells located just beneath the endocardial surface of the left atrial free wall of rat hearts during superfusion and electrical stimulation in vitro at 37°C. 2 Availability of the fast sodium channel for current flow was inferred from the maximum rate of rise of membrane potential during phase O of the action potential ( V̇ max ). 3 Muscle exposed to polysorbate 80 (10 to 80 μg ml −1 ) showed a concentration‐dependent lengthening of action potential duration (APD) but no detectable change in V̇ max . 4 Amiodarone (1 to 20 μg ml −1 ) was dissolved in physiological salt solution with the aid of polysorbate 80 (50 μg ml −1 ) and caused a concentration‐dependent prolongation of APD and a decrease in V̇ max , both of which were slow to develop and extremely slow to wash‐out. The speed of onset of action of amiodarone varied with drug concentration and ranged from a few minutes with high concentrations to many hours with low concentrations.