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Taylor TG, Venable PW, Booth A, et al. Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?. Am J Physiol Heart Circ Physiol. 2013;305(6):H903-12doi: 10.1152/ajpheart.00184.2013.
Taylor, T. G., Venable, P. W., Booth, A., Garg, V., Shibayama, J., & Zaitsev, A. V. (2013). Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?. American journal of physiology. Heart and circulatory physiology, 305(6), H903-12. https://doi.org/10.1152/ajpheart.00184.2013
Taylor, Tyson G, et al. "Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?." American journal of physiology. Heart and circulatory physiology vol. 305,6 (2013): H903-12. doi: https://doi.org/10.1152/ajpheart.00184.2013
Taylor TG, Venable PW, Booth A, Garg V, Shibayama J, Zaitsev AV. Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?. Am J Physiol Heart Circ Physiol. 2013 Sep 15;305(6):H903-12. doi: 10.1152/ajpheart.00184.2013. Epub 2013 Jul 19. PMID: 23873793; PMCID: PMC3761339.
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Am J Physiol Heart Circ Physiol. 2013 Sep 15;305(6):H903-12. doi: 10.1152/ajpheart.00184.2013. Epub 2013 Jul 19.

Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?.

American journal of physiology. Heart and circulatory physiology

Tyson G Taylor, Paul W Venable, Alicja Booth, Vivek Garg, Junko Shibayama, Alexey V Zaitsev

Affiliations

  1. Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah.

PMID: 23873793 PMCID: PMC3761339 DOI: 10.1152/ajpheart.00184.2013

Abstract

Ventricular fibrillation (VF) in the globally ischemic heart is characterized by a progressive electrical depression manifested as a decline in the VF excitation rate (VFR) and loss of excitability, which occur first in the subepicardium (Epi) and spread to the subendocardium (Endo). Early electrical failure is detrimental to successful defibrillation and resuscitation during cardiac arrest. Hyperkalemia and/or the activation of ATP-sensitive K(+) (KATP) channels have been implicated in electrical failure, but the role of these factors in ischemic VF is poorly understood. We determined the VFR-extracellular K(+) concentration ([K(+)]o) relationship in the Endo and Epi of the left ventricle during VF in globally ischemic hearts (Isch group) and normoxic hearts subjected to hyperkalemia (HighK group) or a combination of hyperkalemia and the KATP channel opener cromakalim (HighK-Crom group). In the Isch group, Endo and Epi values of [K(+)]o and VFR were compared in the early (0-6 min), middle (7-13 min), and late (14-20 min) phases of ischemic VF. A significant transmural gradient in VFR (Endo > Epi) was observed in all three phases, whereas a significant transmural gradient in [K(+)]o (Epi > Endo) occurred only in the late phase of ischemic VF. In the Isch group, the VFR decrease and inexcitability started to occur at much lower [K(+)]o than in the HighK group, especially in the Epi. Combining KATP activation with hyperkalemia only shifted the VFR-[K(+)]o curve upward (an effect opposite to real ischemia) without changing the [K(+)]o threshold for asystole. We conclude that hyperkalemia and/or KATP activation cannot adequately explain the heterogeneous electrical depression and electrical failure during ischemic VF.

Keywords: ATP-sensitive potassium channel; asystole; extracellular potassium accumulation; myocardial ischemia; ventricular fibrillation

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