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Increase in Beating Rate of Cultured Chick Cardiac Myocytes by Ethanol and Inhibition of the Increase by Antiarrhythmic Drugs
Author(s) -
Nakamura Kazufumi,
Kouchi Hirosuke,
Ohe Tohru,
Namba Masayoshi
Publication year - 1999
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1999.tb04540.x
Subject(s) - verapamil , disopyramide , myocyte , ethanol , channel blocker , chemistry , quinidine , mexiletine , medicine , pharmacology , endocrinology , antiarrhythmic agent , lidocaine , antagonist , tetraethylammonium , calcium , anesthesia , potassium , receptor , biochemistry , organic chemistry , heart disease
Drinking alcohol sometimes causes cardiac arrhythmia, but the precise mechanism remains unknown. To study the mechanism, we investigated the effects of ethanol exposure on the beating rate of cultured chick cardiac myocytes. Primary cultures of cardiac myocytes were prepared from the ventricles of 14‐day‐old chick embryos and then treated with ethanol which, in the range of 0.3 to 1.5 vol%, increased the beating rate in a dose‐dependent manner. Ethanol (0.6 vol%) caused an increase in the beating rate, but disopyramide (5 μ g/ml) and procainamide (10 μ g/ml), Na + and K + channel blockers, inhibited the increase in the beating rate significantly. Neither lidocaine (5 μ g/ml) nor mexiletine (2 μ g/ml), Na + channel blockers, nor calcium antagonist verapamil (5 ng/ml) inhibited the increase. However, tetraethylammonium chloride (ranging from 15 to 30 mmol/1), a K + channel blocker, inhibited the increase. These findings indicate that ethanol increases the beating rate of cultured chick cardiac myocytes via the activation of the K + channel. This experimental model may be useful in studying the effect of ethanol on the K + channel.