Skip Navigation

Cardiovascular Research 2001 51(1):4-6; doi:10.1016/S0008-6363(01)00335-2
© 2001 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 Dixon, I. M.C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dixon, I. M.C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2000, European Society of Cardiology

Help from within: cardioprotective properties of hepatocyte growth factor

Ian M.C. Dixon*

Department of Physiology, Institute of Cardiovascular Sciences, University of Manitoba, 351 Tache Avenue, Winnipeg, R2H 2A6 Canada

iand@sbrc.ca

* Tel.: +1-204-235-3419; fax: +1-204-233-6723

Received 1 May 2001;
The first 10% of the full text of this article appears below.

See article by Ueda et al. [20] (pages 41–50) in this issue.

Relative volume overload in the aftermath of the acute death of large numbers of cardiac myocytes after myocardial infarction (MI) is causal to progressive cardiac dysfunction. Initially, the myocardium responds to the loss of sarcomeric contractile units with the induction of compensatory cardiac growth. In clinical terms, this response is marked by normalization of wall stress and preservation of pump function within normal limits. The severity of eventual secondary cardiac hypertrophy is variable depending on the initial size of infarction [1,2]. In the event of a large MI, the affected ventricular chamber may undergo dilatation at a point well after the initial insult [3]. At this stage . . . [Full Text of this Article]


   1. Mechanisms of heart failure after myocardial infarction
 

   2. HGF: a novel cardioprotective trophic factor that activates ERK1/2
 

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
 J Ultrasound MedHome page
X. Li, Z. Wang, H. Ran, X. Li, Q. Yuan, Y. Zheng, J. Ren, L. Su, W. Zhang, Q. Li, et al.
Experimental Research on Therapeutic Angiogenesis Induced by Hepatocyte Growth Factor Directed by Ultrasound-Targeted Microbubble Destruction in Rats
J. Ultrasound Med., March 1, 2008; 27(3): 453 - 460.
[Abstract] [Full Text] [PDF]