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Transcript 
Nonequilibrium Reactivation of Na+ Current Drives Early
Afterdepolarizations in Mouse VentricleCLINICAL
PERSPECTIVE
by Andrew G. Edwards, Eleonora Grandi, Johan E. Hake, Sonia Patel, Pan Li,
Shigeki Miyamoto, Jeffrey H. Omens, Joan Heller Brown, Donald M. Bers, and
Andrew D. McCulloch
Circ Arrhythm Electrophysiol
Volume 7(6):1205-1213
December 16, 2014
Copyright © American Heart Association, Inc. All rights reserved.
Calcium calmodulin-dependent protein kinase II delta C (CaMKIIδC)-overexpressing myocytes
are susceptible to early afterdepolarizations (EADs) and sarcoplasmic reticulum (SR) Ca2+
release (SCR).
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
Early afterdepolarization (EAD) susceptibility is associated with exaggerated Ca2+ cycling and
slowed late repolarization.
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
Sarcoplasmic reticulum (SR) Ca2+ release is required for early afterdepolarization (EAD)
initiation.
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
Multiple mechanisms contribute to murine early afterdepolarizations (EADs).
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
INa drives early afterdepolarization (EAD) initiation in murine ventricular myocytes.
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
Nonequilibrium reactivation of INa carries the early afterdepolarization (EAD) upstroke.
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
Simulated calcium calmodulin-dependent protein kinase II (CaMKII) hyperphosphorylation
inhibits rather than promotes nonequilibrium reactivation of INa. A, Simulated action potential
(AP) clamp of the wild-type (WT) and Tg INa models,20 using the first AP with an early
afterdepolarization from the Tg+Iso cell model and showing exaggerated reactivation in the WT
model.
Andrew G. Edwards et al. Circ Arrhythm Electrophysiol.
2014;7:1205-1213
Copyright © American Heart Association, Inc. All rights reserved.
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