Increase in Beating Rate of Cultured Chick Cardiac Myocytes by Ethanol and Inhibition of the Increase by Antiarrhythmic Drugs

Abstract

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 microg/ml) and procainamide (10 microg/ml), Na+ and K+ channel blockers, inhibited the increase in the beating rate significantly. Neither lidocaine (5 microg/ml) nor mexiletine (2 microg/ml), Na+ channel blockers, nor calcium antagonist verapamil (5 ng/ml) inhibited the increase. However, tetraethylammonium chloride (ranging from 15 to 30 mmol/l), 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.

Alcohol‐Induced Reductions in Cardiac Protein Synthesis In Vivo Are Not Ameliorated by Treatment With the Dihydropyridine Calcium Channel Blocker Amlodipine

“…Certainly, in the calcium paradox, verapamil also has been reported to be ineffective (Alanen et al, 1984). In vitro, verapamil does not prevent the arrhythmia effect of alcohol in cultured cardiac myocytes either (Nakamura et al, 1999). When nifedipine is administered chronically to diabetic rats and the hearts are exposed to alcohol acutely (i.e., similar to our protocol for the chronic amlodipine treatments), this calcium channel blocker is able to attenuate the ethanol-induced reduction in peak tension developed (i.e., negative inotropic effect), contraction duration, and maximum velocity of tension development (Brown et al, 1996).…”

Alcohol-Mediated Organ Damages: Heart and Brain

“…Interestingly, no data is available on the electrophysiological effects of low alcohol exposure or on the exposure frequency. Clinically relevant concentrations of ethanol induced elevation of that was dependent on voltage-gated entry into the myocytes through I Ca,L (Brown et al, 1996 ; Solem et al, 2000 ) and reduction in the amplitude of K + currents of rats (Nakamura et al, 1999 ; Dopico, 2003 ; Liu et al, 2003 ). It was shown that the density of dihydropyridine binding sites were greater in cardiomycytes isolated from ethanol-consuming rats as compared to control groups (Brown et al, 1996 ).…”