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Am J Physiol Heart Circ Physiol 278: H677-H687, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 3, H677-H687, March 2000

Beat-to-beat repolarization variability in ventricular myocytes and its suppression by electrical coupling

Massimiliano Zaniboni1, Andrew E. Pollard2, Lin Yang3, and Kenneth W. Spitzer4

1 Department of Evolutive and Functional Biology, University of Parma, Parma, Italy 43100; 2 Department of Biomedical Engineering and Cardiac Rhythm Management Laboratory, University of Alabama at Birmingham, Alabama 35294; 3 Department of Cardiology, First Teaching Hospital, Xian Medical University, Xian, China 710061; and 4 Department of Physiology and Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah 84112-5000

Single ventricular myocytes paced at a constant rate and held at a constant temperature exhibit beat-to-beat variations in action potential duration (APD). In this study we sought to quantify this variability, assess its mechanism, and determine its responsiveness to electrotonic interactions with another myocyte. Interbeat APD90 (90% repolarization) of single cells was normally distributed. We thus quantified APD90 variability as the coefficient of variability, CV = (SD/mean APD90) × 100. The mean ± SD of the CV in normal solution was 2.3 ± 0.9 (132 cells). Extracellular TTX (13 µM) and intracellular EGTA (14 mM) both significantly reduced the CV by 44 and 26%, respectively. When applied in combination the CV fell by 54%. In contrast, inhibition of the rapid delayed rectifier current with L-691,121 (100 nM) increased the CV by 300%. The CV was also significantly reduced by 35% when two normal myocytes were electrically connected with a junctional resistance (Rj) of 100 MOmega . Electrical coupling (Rj = 100 MOmega ) of a normal myocyte to one producing early afterdepolarization (EAD) completely blocked EAD formation. These results indicate that beat-to-beat APD variability is likely mediated by stochastic behavior of ion channels and that electrotonic interactions act to limit temporal dispersion of refractoriness, a major contributor to arrhythmogenesis.

electrotonic interactions; action potential duration; cardiac cells


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