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Does chronic ethanol ingestion alter the acute electrophysiological effects of ethanol on the sinoatrial node in rats?
Does chronic ethanol ingestion alter the acute electrophysiological effects of ethanol on the sinoatrial node in rats?
Chronic ethanol ingestion in rats leads to tolerance to the acute positive chronotropic effects of ethanol on the sinus node without altering responses to carbachol or isoproterenol.
Chronic ethanol induces sinoatrial tolerance in rats; hypothesis-generating and leaves open human relevance.
The influence of moderate chronic ethanol ingestion (CEI) on the acute effects of ethanol upon sinoatrial electrophysiology was studied in rats maintained on a liquid diet for 24 weeks. Rats on ethanol (E-R) received 14% of the caloric intake as ethanol. Controls (N-R) received the same diet, except for isocaloric substitution of carbohydrates for ethanol. The rats were sacrificed at the end of the 24 weeks and sinoatrial preparations were isolated and superfused with Tyrode's solution at 36 degrees C. Intracellular microelectrodes were used to monitor: (a) sinus node automaticity (SNA) in preparations spontaneously active; (b) atrial membrane potentials (AMP) in preparations driven at a constant rate. Ethanol 40-80 mg/100 ml enhanced SNA in N-R, while 240 mg/100 ml were required to obtain a similar effect in E-R. This positive chronotropic effect was not blocked by propranolol. CEI did no modify the effects of carbachol or isoproterenol on SNA. Ethanol 240 mg/100 ml shortened the atrial action potentials in N-R. CEI did not modify the effects of ethanol, carbachol, or isoproterenol on AMP. In summary, small concentrations of ethanol enhanced the SNA in vitro. CEI resulted in development of tolerance to the chronotropic effect of ethanol, without modifying: (a) the acute in vitro effects of carbachol or isoproterenol on SNA and AMP; and (b) the effects of ethanol on AMP.
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Carpentier et al. (1987) studied this question.
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