Cardiac inward rectifier potassium current IK1 is inhibited by
acetaldehyde at clinically relevant concentrations: a role in
arrhythmogenesis related to alcohol consumption?

a 2015

Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption?

BÉBAROVÁ, Markéta; Peter MATEJOVIČ; Milena ŠIMURDOVÁ a Jiří ŠIMURDA

Základní údaje

Originální název

Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption?

Název česky

Srdeční inward rectifier proud IK1 je inhibován acetaldehydem v klinicky relevantních koncentracích: role v arytmogenezi vázané na konzumaci alkoholu?

Autoři

BÉBAROVÁ, Markéta ; Peter MATEJOVIČ; Milena ŠIMURDOVÁ a Jiří ŠIMURDA

Vydání

EHRA Cardiostim 2015, 2015

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

30105 Physiology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Označené pro přenos do RIV

Organizační jednotka

Lékařská fakulta

ISSN

DOI

https://doi.org/10.1093/europace/euv164

Klíčová slova česky

acetaldehyd; IK1; konzumace alkoholu; arytmie

Klíčová slova anglicky

acetaldehyde; IK1; alcohol consumption; arrhythmias

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 23. 11. 2015 10:51, doc. MUDr. Markéta Bébarová, Ph.D.

Anotace

V originále

Purpose: Alcohol intoxication may induce electrocardiographic changes and arrhythmias. Modifications of cardiac inward rectifier potassium currents including IK1 are known to play an important role in the pathogenesis of various types of arrhythmias including those observed under alcohol intoxication. We have recently published a study describing a significant effect of ethanol at clinically relevant concentrations on the ventricular IK1. In the current study, we aimed to analyse changes of the ventricular IK1 in the presence of acetaldehyde, the primary metabolite of ethanol. Methods: Experiments were performed on enzymatically isolated rat ventricular myocytes by the whole cell patch clamp technique at 23 ± 1 °C. IK1 was analysed as the current sensitive to 100 µM Ba2+. Solutions were applied into the near surrounding of the measured cell with a rapid perfusion system. Results: Acetaldehyde (0.3 – 300 µM) induced a reversible inhibition of IK1 with the concentration causing 50% inhibition (IC50) of 53.7 ± 7.7 µM at -100 mV. A significant inhibition was documented even at clinically relevant concentrations; namely 3 µM acetaldehyde reduced IK1 by 13.1 ± 3.0% of. Both development and wash-out of the acetaldehyde effect on IK1 showed a single exponential time course with average time constants of 24.5 ± 3.5 s and 41.5 ± 3.6 s at 3 µM, respectively. The inhibition was voltage-dependent between -120 and -80 mV; at -80 mV and more positive voltages, the inhibition was by about 10% lower than at -100 mV. Conclusions: We conclude that the observed changes of IK1 under clinically relevant concentrations of acetaldehyde might contribute to the alcohol-induced alterations of the cardiac electrophysiology, namely in people with a genetic defect of aldehyde dehydrogenase and, thus, higher plasma levels of acetaldehyde who are often native to Asia.

Návaznosti

NT14301, projekt VaV

Název: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?

Investor: Ministerstvo zdravotnictví ČR, Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?

Citovat

BÉBAROVÁ, Markéta; Peter MATEJOVIČ; Milena ŠIMURDOVÁ a Jiří ŠIMURDA. Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption? In EHRA Cardiostim 2015. 2015. ISSN 1532-2092. Dostupné z: https://doi.org/10.1093/europace/euv164.

@proceedings{1318327,
   author = {Bébarová, Markéta and Matejovič, Peter and Šimurdová, Milena and Šimurda, Jiří},
   booktitle = {EHRA Cardiostim 2015},
   doi = {https://doi.org/10.1093/europace/euv164},
   keywords = {acetaldehyde; IK1; alcohol consumption; arrhythmias},
   language = {eng},
   title = {Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption?},
   year = {2015}
}

TY  - CONF
ID  - 1318327
AU  - Bébarová, Markéta - Matejovič, Peter - Šimurdová, Milena - Šimurda, Jiří
PY  - 2015
TI  - Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption?
KW  - acetaldehyde
KW  - IK1
KW  - alcohol consumption
KW  - arrhythmias
N2  - Purpose: Alcohol intoxication may induce electrocardiographic changes and arrhythmias. Modifications of cardiac inward rectifier potassium currents including IK1 are known to play an important role in the pathogenesis of various types of arrhythmias including those observed under alcohol intoxication. We have recently published a study describing a significant effect of ethanol at clinically relevant concentrations on the ventricular IK1. In the current study, we aimed to analyse changes of the ventricular IK1 in the presence of acetaldehyde, the primary metabolite of ethanol. Methods: Experiments were performed on enzymatically isolated rat ventricular myocytes by the whole cell patch clamp technique at 23 ± 1 °C. IK1 was analysed as the current sensitive to 100 µM Ba2+. Solutions were applied into the near surrounding of the measured cell with a rapid perfusion system. Results: Acetaldehyde (0.3 – 300 µM) induced a reversible inhibition of IK1 with the concentration causing 50% inhibition (IC50) of 53.7 ± 7.7 µM at -100 mV. A significant inhibition was documented even at clinically relevant concentrations; namely 3 µM acetaldehyde reduced IK1 by 13.1 ± 3.0% of. Both development and wash-out of the acetaldehyde effect on IK1 showed a single exponential time course with average time constants of 24.5 ± 3.5 s and 41.5 ± 3.6 s at 3 µM, respectively. The inhibition was voltage-dependent between -120 and -80 mV; at -80 mV and more positive voltages, the inhibition was by about 10% lower than at -100 mV. Conclusions: We conclude that the observed changes of IK1 under clinically relevant concentrations of acetaldehyde might contribute to the alcohol-induced alterations of the cardiac electrophysiology, namely in people with a genetic defect of aldehyde dehydrogenase and, thus, higher plasma levels of acetaldehyde who are often native to Asia.
ER  -

BÉBAROVÁ, Markéta; Peter MATEJOVIČ; Milena ŠIMURDOVÁ a Jiří ŠIMURDA. Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption? In \textit{EHRA Cardiostim 2015}. 2015. ISSN~1532-2092. Dostupné z: https://doi.org/10.1093/europace/euv164.

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