Skip Navigation

Cardiovascular Research 2004 61(3):363-364; doi:10.1016/j.cardiores.2003.12.020
© 2004 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by García-Dorado, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by García-Dorado, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2004, European Society of Cardiology

Myocardial reperfusion injury: a new view

David García-Dorado*,1

Laboratorio de Cardiología Experimental, Servicio de Cardiología, Hospitals Vall d'Hebron, Pg. Vall d'Hebron 119-129, Barcelona 08035, Spain

* Tel.: +34-93-4894038; fax: +34-93-4894032. mrmeana@vhebron.net

Received 18 December 2003; accepted 18 December 2003

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

Acute coronary occlusion resulting in myocardial infarction is the main mechanism by which coronary artery disease reduces survival and leads to deterioration of the quality of life, and the extent of cell death is the main determinant of survival in patients with acute myocardial infarction. Early animal studies demonstrated that once the myocardium becomes severely ischemic, restoration of blood flow is a prerequisite for myocardial salvage. They also showed, however, that restoration of blood flow after transient ischemia may be associated with dramatic, deleterious changes such as arrhythmias, enzyme release, or severe intramyocardial hemorrhage. These changes were generally interpreted as manifestations of . . . [Full Text of this Article]


   1. A new view
 

   2. Therapeutic relevance
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
F. Di Lisa and P. Bernardi
Mitochondria and ischemia-reperfusion injury of the heart: Fixing a hole
Cardiovasc Res, May 1, 2006; 70(2): 191 - 199.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
P. Di Napoli, A. A. Taccardi, A. Grilli, M. A. De Lutiis, A. Barsotti, M. Felaco, and R. De Caterina
Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts
Cardiovasc Res, June 1, 2005; 66(3): 462 - 471.
[Abstract] [Full Text] [PDF]