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      Regional increase in extracellular potassium can be arrhythmogenic due to nonuniform muscle contraction in rat ventricular muscle

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          Abstract

          In the ischemic myocardium, extracellular potassium ([K +] o) increases to ≥20 mmol/l. To determine how lethal arrhythmias occur during ischemia, we investigated whether the increased spatial pattern of [K +] o, i.e., a regional or a global increase, affects the incidence of arrhythmias. Force, sarcomere length, membrane potential, and nonuniform intracellular Ca 2+ ([Ca 2+] i) were measured in rat ventricular trabeculae. A “regional” or “global” increase in [K +] o was produced by exposing a restricted region of muscle to a jet of 30 mmol/l KCl or by superfusing trabeculae with a solution containing 30 mmol/l KCl, respectively. The increase in [Ca 2+] i (Ca CW) during Ca 2+ waves was measured (24°C, 3.0 mmol/l [Ca 2+] o). A regional increase in [K +] o caused nonuniform [Ca 2+] i and contraction. In the presence of isoproterenol, the regional increase in [K +] o induced sustained arrhythmias in 10 of 14 trabeculae, whereas the global increase did not induce such arrhythmias. During sustained arrhythmias, Ca 2+ surged within the jet-exposed region. In the absence of isoproterenol, the regional increase in [K +] o increased Ca CW, whereas the global increase decreased it. This increase in Ca CW with the regional increase in [K +] o was not suppressed by 100 μmol/l streptomycin, whereas it was suppressed by 1) a combination of 10 μmol/l cilnidipine and 3 μmol/l SEA0400; 2) 20 mmol/l 2,3-butanedione monoxime; and 3) 10 μmol/l blebbistatin. A regional but not a global increase in [K +] o induces sustained arrhythmias, probably due to nonuniform excitation-contraction coupling. The same mechanism may underlie arrhythmias during ischemia.

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          Author and article information

          Journal
          Am J Physiol Heart Circ Physiol
          Am. J. Physiol. Heart Circ. Physiol
          ajpheart
          ajpheart
          AJPHEART
          American Journal of Physiology - Heart and Circulatory Physiology
          American Physiological Society (Bethesda, MD )
          0363-6135
          1522-1539
          1 June 2012
          23 March 2012
          1 June 2013
          : 302
          : 11
          : H2301-H2309
          Affiliations
          [1] 1Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine, Sendai, Japan; and
          [2] 2Department of Pharmacology, Columbia College of Physicians and Surgeons, New York, New York
          Author notes
          Address for reprint requests and other correspondence: M. Miura, Dept. of Clinical Physiology, Health Science, Tohoku Univ. Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan (e-mail: mmiura@ 123456med.tohoku.ac.jp ).
          Article
          PMC3378298 PMC3378298 3378298 H-01161-2011
          10.1152/ajpheart.01161.2011
          3378298
          22447939
          21ae59d9-5d40-4338-a289-415d8cd81fa8
          Copyright © 2012 the American Physiological Society
          History
          : 15 December 2011
          : 18 March 2012
          Categories
          Cardiac Excitation and Contraction

          calcium waves,ischemia,calcium,high extracellular potassium

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