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Cardiovascular Research 2007 74(3):341-342; doi:10.1016/j.cardiores.2007.04.003
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Copyright © 2007, European Society of Cardiology

Gap junctions in preconditioning against arrhythmias

Elena C. Lascano* and Jorge A. Negroni

Department of Physiology, Pharmacology and Biochemistry, Favaloro University, Solís 453, 1078 Buenos Aires, Argentina

* Corresponding author. Tel.: +54 11 4378 1187; fax: +54 11 4381 0323. Email address: lascano@favaloro.edu.ar

Received 26 March 2007; accepted 2 April 2007

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

See article by Papp et al. [10] (pages 396–405) in this issue.

Ischemic preconditioning is a natural mechanism by which brief periods of ischemia–reperfusion initiate a complex cascade of events that culminate in the protection of the heart against a subsequent sustained ischemia, reducing infarct size, postischemic dysfunction, and the incidence of arrhythmias [1]. In essence, endogenous or exogenous triggers released during ischemic or pharmacological preconditioning activate mediators that act on end-effectors, preserving mitochondrial, cytoskeletal, and cell membrane integrity [2]. However, although much effort has been dedicated to the study of preconditioning mechanisms, these have not been clearly . . . [Full Text of this Article]


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