Key result
Alpha-1 and beta-1 adrenoceptor stimulation enhanced automaticity through different mechanisms in guinea pig pulmonary vein myocardium, and carvedilol significantly inhibited noradrenaline-induced activity.
Why the study?
Does dual blockade of alpha- and beta-adrenoceptors suppress noradrenaline-induced automaticity in guinea pig pulmonary vein myocardium?
Population
Isolated guinea pig pulmonary vein myocardium tissue preparations
Comparison
Application of adrenoceptor agonists and… vs Baseline quiescent state or preparations driven…
Design
Preclinical
Authors
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Supports carvedilol investigation for AF triggers; hypothesis-generating in vitro data requiring clinical validation.
Does dual blockade of alpha- and beta-adrenoceptors suppress noradrenaline-induced automaticity in guinea pig pulmonary vein myocardium?
Dual blockade of alpha-1 and beta-1 adrenoceptors effectively suppresses noradrenaline-induced pulmonary vein automaticity, highlighting a potential pharmacological strategy for preventing atrial fibrillation.
Irie et al. (2017) studied Atrial fibrillation (mechanism). Adrenoceptor agonists and antagonists (noradrenaline, carvedilol, bisoprolol, etc.) was evaluated on Automatic activity (firing frequency and membrane potential). Alpha-1 and beta-1 adrenoceptor stimulation enhanced automaticity through different mechanisms in guinea pig pulmonary vein myocardium, and carvedilol significantly inhibited noradrenaline-induced activity.
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