a 2025

Aminophylline at clinically relevant concentrations affects inward rectifier potassium current in healthy porcine and failing human cardiomyocytes in a similar manner

BÉBAROVÁ, Markéta; Olga ŠVECOVÁ; Roman KULA; Michal PÁSEK; Edita JEKLOVA et al.

Základní údaje

Originální název

Aminophylline at clinically relevant concentrations affects inward rectifier potassium current in healthy porcine and failing human cardiomyocytes in a similar manner

Vydání

XXXIII. VÝROČNÍ SJEZD ČESKÉ KARDIOLOGICKÉ SPOLEČNOSTI, 2025

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

30201 Cardiac and Cardiovascular systems

Stát vydavatele

Česká republika

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/25:00141204

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

Aminophylline;Arrhythmia;Inward rectifier;Action potential;Pig;Human

Štítky

Změněno: 16. 3. 2026 13:30, Mgr. Tereza Miškechová

Anotace

V originále

Aminophylline, a bronchodilator mainly used to treat severe asthma attacks, may induce arrhythmias. Unfortunately, the underlying mechanism is not well understood. We have recently described a significant, on average inhibitory effect of aminophylline on inward rectifier potassium current IK1, known to substantially contribute to arrhythmogenesis, in rat ventricular myocytes at room temperature. This study was aimed to examine whether a similar effect may be observed under clinically relevant conditions. Experiments were performed using the whole cell patch clamp technique at 37◦C on enzymatically isolated healthy porcine and failing human ventricular myocytes. The effect of clinically relevant concentrations of aminophylline (10–100 µM) on IK1 did not significantly differ in healthy porcine and failing human ventricular myocytes. IK1 was reversibly inhibited by ~20 and 30 % in the presence of 30 and 100 µM aminophylline, respectively, at 110 mV; an analogical effect was observed at -50 mV. To separate the impact of IK1 changes on AP configuration, potentially interfering ionic currents were blocked (L-type calcium and delayed rectifier potassium currents). A significant prolongation of AP duration was observed in the presence of 100 µM aminophylline in porcine cardiomyocytes which well agreed with the effect of a specific IK1 inhibitor Ba2+ (10 µM) and with the result of simulations using a porcine ventricular cell model. We conclude that the observed effect of aminophylline on healthy porcine and failing human IK1 might be involved in its proarrhythmic action. To fully understand the underlying mechanism, potential aminophylline impact on other ionic currents should be explored.

Návaznosti

LX22NPO5104, projekt VaV
Název: Národní institut pro výzkum metabolických a kardiovaskulárních onemocnění (Akronym: CarDia)
Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Národní institut pro léčbu metabolických a kardiovaskulárních onemocnění, 5.1 EXCELES