Key result
Aconitine inhibited delayed-rectifier and inwardly rectifying K+ currents, induced early after-depolarizations in vitro, and caused prolonged QT intervals and polymorphic ventricular tachycardia in vivo.
Why the study?
To investigate the electrophysiological effects of aconitine on ion currents, cardiac action potentials, and arrhythmogenic properties.
Does aconitine alter membrane currents and action potentials in neonatal rat ventricular myocytes and induce electrocardiographic changes in rats?
Population
Neonatal rat ventricular myocytes and Sprague-Dawley rats
Comparison
Aconitine exposure vs baseline
Design
Preclinical in vitro and in vivo electrophysiological study
Authors
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Aconitine induces proarrhythmic changes in rat myocytes; hypothesis-generating for human toxicity and requires clinical validation.
Does aconitine alter membrane currents and action potentials in neonatal rat ventricular myocytes and induce electrocardiographic changes in rats?
Aconitine exhibits significant arrhythmogenic properties by inhibiting potassium currents and inducing early after-depolarizations, leading to prolonged QT and polymorphic ventricular tachycardia.
Chou et al. (2024) studied Cardiac electrophysiology (preclinical). Aconitine vs. Control (no aconitine) was evaluated on Electrophysiological changes (ion currents, action potentials, and ECG). Aconitine inhibited delayed-rectifier and inwardly rectifying K+ currents, induced early after-depolarizations in vitro, and caused prolonged QT intervals and polymorphic ventricular tachycardia in vivo.
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