© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Injury current modulates afterdepolarizations in single human ventricular cells
aDepartment of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
bDepartment of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
cDepartment of Cardiology, Academic Medical Center, University Medical Center Utrecht, Utrecht, The Netherlands
dDepartment of Medical Physiology and Sports Medicine, University Medical Center Utrecht, Utrecht, The Netherlands
* Corresponding author. Tel.: +31-20-566-4670; fax: +31-20-691-9319 A.O.Verkerk{at}amc.uva.nl
Objective: Injury current (Iinjury) and afterdepolarizations are thought to play an important role in arrhythmias that occur during acute ischemia. However, little is known about the effects of Iinjury on afterdepolarizations. The present study was designed to study the effect of Iinjury on afterdepolarizations and action potentials in single human ventricular cells. Methods: The patch-clamp technique was used to record action potentials and to apply Iinjury to human ventricular cells. In these cells, early and delayed afterdepolarizations (EADs and DADs) were induced by 1 µM norepinephrine. Iinjury was simulated by coupling cells via a variable coupling resistance to a passive resistance circuit with a potential of 0, –20, or –40 mV, mimicking a depolarized ischemic region. Results: At all potentials, Iinjury induced depolarization of the resting membrane potential and action potential shortening. Flowing from 0 mV, Iinjury induced EADs by itself and aggravated the EADs and DADs that were induced by norepinephrine. Flowing from –40 mV, Iinjury abolished the noradrenaline-induced EADs and DADs. Conclusions: Our results demonstrate that Iinjury may either prevent or promote the occurrence of afterdepolarizations in human ventricle. The latter holds if conduction is slowed to such an extent that it permits flow of current from depolarized ischemic cells at plateau level to cells in phase 3 or phase 4.
KEYWORDS Arrhythmia (mechanisms); Cell communication; Impulse formation; Ischemia; Membrane potential
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