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Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution.

Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Research Abstract Details 

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  • Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Abstract Text:

     knollmann Knollmann,tilmann schoberTilmann Schober,andreas o petersenAndreas O Petersen,syevda g sirenkoSyevda G Sirenko,michael r franzMichael R Franz,

    Transgenic mice have been increasingly utilized to investigate the molecular mechanisms of cardiac arrhythmias, yet the rate dependence of the murine action potential duration and the electrical restitution curve (ERC) remain undefined. In the present study, 21 isolated, Langendorff-perfused, and atrioventricular node-ablated mouse hearts were studied. Left ventricular and left atrial action potentials were recorded using a validated miniaturized monophasic action potential probe. Murine action potentials (AP) were measured at 30, 50, 70, and 90% repolarization (APD(30)-APD(90)) during steady-state pacing and varied coupling intervals to determine ERCs. Murine APD showed rate adaptation as well as restitution properties. The ERC time course differed dramatically between early and late repolarization: APD(30) shortened with increasing S1-S2 intervals, whereas APD(90) was prolonged. When fitted with a monoexponential function, APD(30) reached plateau values significantly faster than APD(90) (tau = 29 +/- 2 vs. 78 +/- 6 ms, P < 0.01, n = 12). The slope of early APD(90) restitution was significantly <1 (0.16 +/- 0.02). Atrial myocardium had shorter final repolarization and significantly faster ERCs that were shifted leftward compared with ventricular myocardium. Recovery kinetics of intracellular Ca(2+) transients recorded from isolated ventricular myocytes at 37 degrees C (tau = 93 +/- 4 ms, n = 18) resembled the APD(90) ERC kinetics. We conclude that mouse myocardium shows AP cycle length dependence and electrical restitution properties that are surprisingly similar to those of larger mammals and humans.

    Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Publishing Authors By Initials

    bc knollmannBC Knollmann,t schoberT Schober,ao petersenAO Petersen,sg sirenkoSG Sirenko,mr franzMR Franz,

    For similar musculoskeletal, neural, and ocular physiology: nervous system physiology: nervous system physiologic phenomena: refractory period, electrophysiological research abstracts see: musculoskeletal, neural, and ocular physiology: nervous system physiology: nervous system physiologic phenomena: refractory period, electrophysiological research

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    Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Heart and circulat

    VOLUME: 292

    Page Numbers: H614-21

    Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

    ISSN: 0363-6135

    DAY: 8

    MONTH: 09

    YEAR: 2006

    Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901228

    Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Keywords Mesh Terms:

    KEYWORDS: Refractory Period, Electrophysiological

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Information

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    Grant and Affiliation Information for Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution.

    AFFILIATION: Oates Institute for Experimental Therapeutics, Vanderbilt Univ. School of Medicine, Division of Clinical Pharmacology, 1265 Medical Research Bldg. IV, Nashville, TN 37232-0575, USA. bjorn.knollmann@vanderbilt.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R01 HL-71670

    ACRONYM: HL

    MEDLINETA: Am J Physiol Heart Circ Physio

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