Key result
In murine ventricular myocytes, nonequilibrium reactivation of Na+ current drives early afterdepolarizations, with lidocaine (40-60 μmol/L) eliminating virtually all EAD-elicited inward current.
Population
Myocytes from arrhythmia-susceptible calcium calmodulin-dependent protein kinase II delta C-overexpressing…
Design
Preclinical
Authors
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Challenges ICaL-centric EAD models in mice; leaves open Na+ current role in human arrhythmia mechanisms.
This study demonstrates that unlike in large mammals, early afterdepolarizations in mice are driven by nonequilibrium reactivation of sodium current rather than L-type calcium current, which is critical for interpreting arrhythmia mechanisms in murine models.
Edwards et al. (2014) studied Cardiac arrhythmia / Early afterdepolarizations. Pharmacological agents (lidocaine, caffeine, tetrodotoxin) was evaluated on Early afterdepolarization (EAD) initiation and inward current. In murine ventricular myocytes, nonequilibrium reactivation of Na+ current drives early afterdepolarizations, with lidocaine (40-60 μmol/L) eliminating virtually all EAD-elicited inward current.
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