Abstract
We have studied the dependence of conduction velocity (θ) on extracellular potassium concentration ([K+]o) in a model of one-dimensional conduction using an idealized strand of human atrial cells. Elevated [K+]o in the 5–20 mM range shifts the resting potential (V rest) in the depolarizing direction and reduces input resistance (R in) by increasing an inwardly rectifying K+ conductance, I Kl.Our results show that in this model: (1) θ depends on [K+] in a “biphasic” fashion. Moderate elevations of [K+]o (to less than 8 mM) result in a small increase in θ, whereas at higher [K+]o (8–16 mM) θ is reduced. (2) This biphasic relationship can be attributed to the competing effects of (i) the smaller depolarization needed to reach the excitation threshold (V thresh-V rest) and (ii) reduced availability (increased inactivation) of sodium current, I Na, as the cell depolarizes progressively. (3) Decreasing R in reduces θ due to the increased electrical load on surrounding cells. (4) The effect on θ of [K+]o-induced changes in R inin the atrium (as well as other high-R in tissue, such as that of the Purkinje system or nodes) is likely to be small. This effect could be substantial, however, under conditions in which R in is comparable in size to gap junction resistance and membrane resistance (inverse slope of the whole-cell current–voltage relationship) when sodium channels are open, which is likely to be the case in ventricular tissue. © 2000 Biomedical Engineering Society.PAC00: 8716Uv, 8719Hh, 8716Ac
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Nygren, A., Giles, W.R. Mathematical Simulation of Slowing of Cardiac Conduction Velocity by Elevated Extracellular [K+] in a Human Atrial Strand. Annals of Biomedical Engineering 28, 951–957 (2000). https://doi.org/10.1114/1.1308489
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DOI: https://doi.org/10.1114/1.1308489