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Cardiovascular Research 2005 66(1):9-11; doi:10.1016/j.cardiores.2005.02.003
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Copyright © 2005, European Society of Cardiology

Hypoxia, electrical uncoupling, and conduction slowing: Role of conduction reserve

Harold V.M. van Rijena,*, Jacques M.T. de Bakkerb,c,d and Toon A.B. van Veena

aDepartment of Medical Physiology, University Medical Center Utrecht, Yalelaan 50, 3584CM Utrecht, The Netherlands
bInteruniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
cHeart Lung Center Utrecht, University Medical Center, Utrecht, The Netherlands
dExperimental and Molecular Cardiology, Academic Medical Center, Amsterdam, The Netherlands

* Corresponding author. Tel.: +31 302538900; fax: +31 302539036. Email address: H.V.M.vanRijen@med.uu.nl

Received 31 January 2005; accepted 3 February 2005

The first 10% of the full text of this article appears below.

See article by Zeevi-levin et al. [7] (pages 64–73) in this issue.

Cardiac activation is based on propagation of the action potential and requires low resistance cell–cell coupling and proper excitability. The electrical coupling between myocytes is mediated by protein channels, called gap junctions, consisting of connexins (Cx, in the ventricle mainly Cx43). Sodium channels (SCN5A) are the major channel proteins involved in excitability of the cardiac cells. A third factor that determines conduction velocity is the tissue architecture, which involves cell shape [1] and interstitial collagen content (fibrosis) [2]. Many cardiac pathologies change these determinants, which give rise to slow and abnormal conduction and increases the propensity for arrhythmias.

Myocardial ischemia is strongly . . . [Full Text of this Article]


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