| Changes in anisotropic conduction caused by remodeling cell size and the cellular distribution of gap junctions and Na(+) channels. | |
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MedLine Citation:
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PMID: 11781939 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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(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(max) was not different during longitudinal and transverse propagation. However, growth hypertrophy produced a selective increase in mean transverse V(max) with no significant change in longitudinal V(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 gap junctions is important in sustaining a maximum rate of rise of the action potential. |
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Authors:
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M S Spach; J F Heidlage; P C Dolber; R C Barr |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of electrocardiology Volume: 34 Suppl ISSN: 0022-0736 ISO Abbreviation: J Electrocardiol Publication Date: 2001 |
Date Detail:
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Created Date: 2002-01-08 Completed Date: 2002-02-13 Revised Date: 2009-11-11 |
Medline Journal Info:
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Nlm Unique ID: 0153605 Medline TA: J Electrocardiol Country: United States |
Other Details:
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Languages: eng Pagination: 69-76 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA. cspach@duke.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials Animals Animals, Newborn Anisotropy Connexin 43 / analysis Dogs Gap Junctions / physiology* Heart / growth & development Myocardium / cytology Sodium Channels / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Connexin 43; 0/Sodium Channels |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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