Abstract
Potassium and Anisotropy. Introduction: The purpose of this study was to investigate the effects of potassium on anisotropic conduction in rabbit ventricles. Methods and Results: In Langendorff perfused rabbit hearts, a two‐dimensional epicardial layer of anisotropic myocardium was created by cryodestruction of the endocardial four fifths of the left ventricle. The heart was paced at 0.5 Hz and the epicardial spread of activation was recorded with a high‐resolution mapping electrode (240 points). In ten experiments, we studied the effects of stepwise increased concentrations of extracellular potassium on epicardial conduction, longitudinal and transverse to the fiber direction. At 6.2 mM of K+, longitudinal conduction velocity (θL) was 61 ± 6.2 and transverse conduction velocity (θT) 25 ± 4.6 cm/sec with a ratio θL/θT of 2.6. At a high concentration of 12.5 ± 1.1 mM, conduction slowed down to 29 ± 6.0 and 11 ± 4.4 cm/sec, respectively, with a slightly increased ratio of 3.2 (NS). The amount of depression of θL and θT varied considerably from experiment to experiment and from region to region. On the average, no statistical difference in the depression of conduction velocity in relation to the fiber orientation was found. At K + concentrations of more than 12.5 ± 1.1 mM, local conduction was seriously impaired at various sites. Lines of functional conduction block appeared in longitudinal and transverse direction. Conclusion: We conclude that during slow heart rates, depression of the fast sodium channels by high extracellular K + causes no detectable differential effects on conduction velocity or on occurrence of conduction block, longitudinal or transverse to the general fiber orientation.
Published Version
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