4.1 Article Proceedings Paper

Changes in anisotropic conduction caused by remodeling cell size and the cellular distribution of gap junctions and Na+ channels

期刊

JOURNAL OF ELECTROCARDIOLOGY
卷 34, 期 -, 页码 69-76

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CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
DOI: 10.1054/jelc.2001.28833

关键词

gap junctions; anisotropic propagation; V-max; structural remoleling; cellular size

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Because gene therapy presents a new frontier in the treatment of arrhythmias, it has become important to know how manipulation of the cellular distribution of proteins changes electrical events within individual cells, and whether these cellular changes affect conduction at the larger macroscopic size scale. However, experimental limitations in cardiac bundles prevent measurement of conduction delays across specific gap junctions, as well as the intracellular distribution of the maximum rate of rise of the action potential (V(over dot)(max)). In view of these limitations, we used immunohistochemical morphological results as a basis to develop two-dimensional cellular models of neonatal and mature canine ventricular muscle in order to obtain insight into the electrophysiological effects of changes in the cellular distribution of proteins; eg, the major protein of cardiac gap junctions, connexin43. Morphological results showed that when the cells enlarged after birth, the gap junctions shifted from the sides to the ends of ventricular myocytes. At birth, V(over dot)(max) was not different during longitudinal and transverse propagation. However, growth hypertrophy Produced a selective increase in mean transverse V(over dot)(max) with no significant change in longitudinal V(over dot)(max). Two-dimensional cellular computational models of neonatal and mature ventricular muscle showed that the observed changes in the cellular distribution of the gap junctions and change in cell size accounted for the experimental results. The results unexpectedly showed that cellular scaling cell size) is as important (or more so) as changes in gap junction distribution in determining the properties of transverse propagation. The results suggest that in pathological states that are arrhythmogenic, maintenance of cell size during remodeling the distribution of gal) junctions is important in sustaining a maximum rate of rise of the action potential.

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