Effects of chronic atrial fibrillation on gap junction distribution in human and rat atria

Détails

ID Serval
serval:BIB_5E8300EA6795
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Effects of chronic atrial fibrillation on gap junction distribution in human and rat atria
Périodique
Journal of the American College of Cardiology
Auteur(s)
Polontchouk  L., Haefliger  J. A., Ebelt  B., Schaefer  T., Stuhlmann  D., Mehlhorn  U., Kuhn-Regnier  F., De Vivie  E. R., Dhein  S.
ISSN
0735-1097 (Print)
Statut éditorial
Publié
Date de publication
09/2001
Volume
38
Numéro
3
Pages
883-91
Notes
In Vitro
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep
Résumé
OBJECTIVES: To elucidate the structural basis for the electrophysiologic remodeling induced by chronic atrial fibrillation (AF), we investigated connexin40 and connexin43 (Cx40 and Cx43) expression and distribution in atria of patients with and without chronic AF and in an animal model of AF with additional electrophysiologic investigation of anisotropy (ratio of longitudinal and transverse velocities). BACKGROUND: Atrial fibrillation is a common arrhythmia that has a tendency to become persistent. Since gap junctions provide the syncytial properties of the atrium, changes in expression and distribution of intercellular connections may accompany the chronification of AF. METHODS: Atrial tissues isolated from 12 patients in normal sinus rhythm at the time of cardiac surgery and from 12 patients with chronic AF were processed for immunohistology and immunoblotting for the detection of the gap junction proteins. The functional study of the cardiac tissue anisotropy was performed in rat atria in which AF was induced by 24 h of rapid pacing (10 Hz). RESULTS: Immunoblotting revealed that AF did not induce any significant change in Cx43 content in human atria. In contrast, a 2.7-fold increase in expression of Cx40 was observed in AF. Immunohistologic analysis indicated that AF resulted in an increase in the immunostaining of both connexins at the lateral membrane of human atrial cells. A similar spatial redistribution of the Cx43 signal was seen in isolated rat atria with experimentally-induced AF. In addition, AF in rat atria resulted in decreased anisotropy with slightly enhanced transverse conduction velocity. CONCLUSIONS: This experimental study showed that AF is accompanied by spatial remodeling of gap junctions that might induce changes in the biophysical properties of the tissue.
Mots-clé
Aged Animals Anisotropy Atrial Fibrillation/*metabolism Blotting, Western Chronic Disease Connexin 43/*metabolism Connexins/*metabolism Electrophysiologic Techniques, Cardiac Gap Junctions/*metabolism Heart Atria/*metabolism Humans Immunohistochemistry Middle Aged Models, Animal Rats Tissue Distribution
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 14:47
Dernière modification de la notice
20/08/2019 15:16
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