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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/H614    most recent 01085.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Knollmann, B. C. Articles by Franz, M. R. Search for Related Content PubMed PubMed Citation Articles by Knollmann, B. C. Articles by Franz, M. R.

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

¹Oates Institute for Experimental Therapeutics and Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee; and ²Department of Pharmacology, Georgetown University Medical Center, and ³Division of Cardiology, Veterans Affairs Medical Center, Washington, District of Columbia

Submitted 13 October 2005 ; accepted in final form 5 September 2006

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 (APD₃₀–APD₉₀) 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: APD₃₀ shortened with increasing S1–S2 intervals, whereas APD₉₀ was prolonged. When fitted with a monoexponential function, APD₃₀ reached plateau values significantly faster than APD₉₀ ( = 29 ± 2 vs. 78 ± 6 ms, P < 0.01, n = 12). The slope of early APD₉₀ 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 Ca²⁺ transients recorded from isolated ventricular myocytes at 37°C ( = 93 ± 4 ms, n = 18) resembled the APD₉₀ 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.

atrium; ventricle; monophasic action potential; calcium transients

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