Protective role of salbutamol against aminophylline-induced arrhythmias in an hPSC-based cardiac model

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Publikace nespadá pod Ústav výpočetní techniky, ale pod Lékařskou fakultu. Oficiální stránka publikace je na webu muni.cz.
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SCUREK Martin KABANOV Daniil KLIMOVIC Simon BECKEROVA Deborah PEŠL Martin PRIBYL Jan BÉBAROVÁ Markéta ROTREKL Vladimír BRAT Kristian

Rok publikování 2025
Druh Stať ve sborníku
Konference EUROPEAN RESPIRATORY JOURNAL
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
www https://publications.ersnet.org/content/erj/66/suppl69/pa1410
Doi https://doi.org/10.1183/13993003.congress-2025.PA1410
Klíčová slova Cellular biosensor; atomic force microscopy; arrhythmia; cardiomyocytes; drug screening; drug cardiotoxicity; conduction; pluripotent stem cells; biomechanical properties.
Popis Introduction: Aminophylline and salbutamol are commonly used in clinical practice to treat obstructive lung diseases. While the adverse effects of individual bronchodilators, including arrhythmias, are well-documented, the potential side effects of their combined use remain largely unknown. Aims: This study aimed to evaluate the arrhythmogenic potential of aminophylline and salbutamol co-administration in vitro. Methods: We used an established atomic force microscopy (AFM) model integrated with cardiac organoids derived from human pluripotent stem cells (hPSC-CMs). The study focused on assessment of chronotropic, inotropic, and arrhythmogenic effects of salbutamol alone and in combination with aminophylline. To detect arrhythmic events, we employed heart rate/beat rate variability (HRV/BRV) analysis in AFM recordings from hPSC-CMs. Results: Salbutamol reduced aminophylline-induced arrhythmogenicity, likely through endothelial nitric oxide synthase activation via beta-2 adrenergic receptors. These findings were validated using hPSC-CMs derived from two distinct cell lines (CCTL4 and CCTL12). Conclusion: Our results suggest that salbutamol, beyond its bronchodilator properties, may increase the cardiovascular safety of aminophylline by reducing its arrhythmogenic potential.
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