Ethanol as an arrhythmogen and an antiarrhythmic agent with reoxygenation arrhythmias of cultured heart cells

Wenzel, Duane G.; Fuh, I. Y.

doi:10.1007/bf01967629

Cited by 4 publications

(1 citation statement)

References 24 publications

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“…Anti-fibrillatory effects of ethanol have also been reported [23,28]. Finally, cardio-protective effects (i.e., infarct size) of ethanol during ischemia and reperfusion/reoxygenation have been shown in anesthetized guinea pig and rat models [2,30], isolated perfused rat hearts [2] and cultures of neonate rat cardiomyocytes [40].…”

Section: Introductionmentioning

confidence: 96%

Ethanol protects against lysophosphatidylcholine-induced uncoupling of cardiac cell pairs

Daleau

2002

Pfl�gers Archiv European Journal of Physiology

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Moderate alcohol consumption is related to a reduction in cardiovascular deaths. Lysophosphatidylcholine (LPC) produces arrhythmias similar to those induced by ischemia most likely due to its uncoupling properties. We assessed effects of LPC in the presence of ethanol in cardiac myocyte pairs using the double whole-cell voltage-clamp technique. Ethanol 11, 22 and 44 mmol.l(-1) did not change junctional conductance for up to 25 min but postponed the time for total uncoupling induced by 20 micromol.l(-1) LPC from 11.3+/-3.0 min ( n=4), respectively, to 16.0+/-0.5 ( n=3; P=0.05), 20.5+/-1.9 min ( n=4; P<0.05) and 27.0+/-3.5 min ( n=3; P=0.01; mean+/-SEM). LPC-induced uncoupling which might occur during ischemia may be counteracted by ethanol.

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Section: Introductionmentioning

confidence: 96%

Ethanol protects against lysophosphatidylcholine-induced uncoupling of cardiac cell pairs

Daleau

2002

Pfl�gers Archiv European Journal of Physiology

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Decrease of epinephrine-induced arrhythmia threshold in ethanol exposed rats

1992

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An association between cardiac arrhythmias and ethanol use has been observed for some time. The sympathetic nervous system presumably plays an important role in the manifestation of cardiovascular ethanol responses. Therefore, we investigated the effects of ethanol treatment on epinephrine-induced arrhythmias. Female Wistar rats received 10 vol% ethanol or 2.5% glucose (control group) in their drinking water for 45 days. In ether anesthetized animals of both groups epinephrine (10 micrograms/kg.min) was infused via a lateral tail vein. The threshold dose for arrhythmias after epinephrine infusion (mainly 2nd and 3rd degree AV-blocks) was reduced beginning 2 days after the start of the ethanol treatment and the incidence of AV-blocks during epinephrine infusion was increased. During the ethanol treatment the prohypertensive epinephrine effect was slightly increased. The reflex bradycardia was not changed after repeated epinephrine infusion by ethanol treatment, whereas it was nearly abolished in the control group. No blood ethanol could be detected during the time of epinephrine infusion (9-12 a.m.), but determinations at 11 p.m. yielded a concentration of 0.13 +/- 0.02 mg/g. The results show that the epinephrine-induced bradyarrhythmia threshold is reduced and the frequency of arrhythmic events is augmented in rats exposed to ethanol in the drinking fluid.

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