Key result
Selective activation of I(Ks) by L3 attenuated prolonged action potentials and eliminated early afterdepolarizations in control and hypertrophied rabbit ventricular myocytes.
Why the study?
Does pharmacological activation of I(Ks) by L3 correct abnormal repolarization and eliminate early afterdepolarizations in rabbit models of acquired LQT2 and ventricular hypertrophy?
Population
Rabbit ventricular myocytes (control, dofetilide-treated, and hypertrophied models)
Comparison
L3 (a new benzodiazepine I(Ks) activator) vs Control conditions (absence of L3)
Design
Preclinical
Authors
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May inform I(Ks) activator development for long QT and hypertrophy; hypothesis-generating from rabbit data and should not yet change practice.
Does pharmacological activation of I(Ks) by L3 correct abnormal repolarization and eliminate early afterdepolarizations in rabbit models of acquired LQT2 and ventricular hypertrophy?
Pharmacological activation of I(Ks) with L3 corrects abnormal repolarization and suppresses early afterdepolarizations in rabbit models, suggesting a potential strategy for treating arrhythmias in long QT syndrome or cardiac hypertrophy.
Xu et al. (2002) studied Acquired LQT2 and ventricular hypertrophy (rabbit models). I(Ks) activation by a new benzodiazepine (L3) vs. Control myocytes was evaluated on Action potential (AP) prolongation and early afterdepolarizations (EAD). Selective activation of I(Ks) by L3 attenuated prolonged action potentials and eliminated early afterdepolarizations in control and hypertrophied rabbit ventricular myocytes.
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