Nom du corpus

Corpus Systématique Animale

Titre du document

Sotalol facilitates spontaneous ventricular defibrillation by enhancing intercellular coupling. An entirely new mechanism for its antiarrhythmic action

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Éditeur
Springer (journals)
Langue(s) du document
Anglais
Type de document
Research-article
Mots-clés d'auteur
  • Sotalol
  • Intercellular coupling
  • Spontaneous ventricular defibrillation
  • Guinea pig
Nom du fichier dans la ressource
Mammiferes_v2b_01399
Auteur(s)
  • H. Uchiyama 1
  • M. Manoach 1,2
  • E. Miyachi 3
  • Y. Watanabe 1
Affiliation(s)
  • 1) Cardiovascular Institute, Fujita Health University, 470-11, Toyoake, Aichi, Japan
  • 2) Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
  • 3) Second Department of Physiology, Fujita Health University, 470-11, Toyoake, Aichi, Japan
Résumé

We have previously shown that sotalol, a class III antiarrhythmic agent, helps spontaneous ventricular defibrillation in various mammalian species. Since we hypothesized that self ventricular defibrillation depends on a high degree of intercellular synchronization, and since the major electrophysiological action of sotalol causing prolongation of action potential duration (APD), cannot fully explain its defibrillating property, we carried out a series of studies to examine the effect of sotalol on intercellular myocardial coupling. Guinea pig right ventricular muscle preparations were superfused in a tissue bath and the spread of intracellularly injected fluorescent dye (Lucifer yellow CH) to the neighboring cells was studied under various conditions. When either the Ca2+ concentration of Tyrode's solution was elevated to 6 mM or the solution was made hypoxic by not bubbling O2 (n = 3 each), no spread of the injected dye was observed. The addition of 1 µM sotalol to the high Ca2+ solution or 0.5 µM to the hypoxic superfusate (n = 3 each) caused a wide spreading of the dye, thus strongly suggesting a marked improvement in the intercellular coupling. These results show an entirely new property of sotalol, i.e., enhancement of cellular synchronization, which may better explain its ability to cause spontaneous ventricular defibrillation than its class III action. Our previous demonstration of successful spontaneous ventricular defibrillation by several other agents that are known to enhance intercellular coupling but have contrasting actions on APD further substantiates our hypothesis.

Catégories Science-Metrix
  • 1 - health sciences
  • 2 - clinical medicine
  • 3 - cardiovascular system & hematology
Catégories INIST
  • 1 - sciences appliquees, technologies et medecines
  • 2 - sciences biologiques et medicales
  • 3 - sciences medicales
Catégories Scopus
  • 1 - Health Sciences ; 2 - Medicine ; 3 - Cardiology and Cardiovascular Medicine
Catégories WoS
  • 1 - science ; 2 - peripheral vascular disease
  • 1 - science ; 2 - cardiac & cardiovascular systems
Identifiant ISTEX
A4A8FCE37B2410620CB5A078206DDB7FB8BD08E7
Revue

Heart and Vessels

Année de publication
1995
Présence de XML structuré
Non
Version PDF
1.3
Score qualité du texte
7.63
Sous-corpus
  • Mammiferes
Type de publication
Journal
ark:/67375/1BB-60P27D16-K
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