Skip Navigation

European Heart Journal 1995 16(2):243-252;
Copyright © 1995 by the European Society of Cardiology.
This Article
Right arrow Full Text (PDF)
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 HERRMANN, H. J.
Right arrow Articles by BLÖDNER, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HERRMANN, H. J.
Right arrow Articles by BLÖDNER, R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1995 The European Society of Cardiology

Pathogenesis of myocardial fibrosis in spontaneously hypertensive rats (SHR)

H. J. HERRMANN*,{maltese cross}, U. FIEDLER* and R. BLÖDNER{dagger}

*Max Delbrück Centre of Molecular Medicine Berlin
{maltese cross}The first author of this paper died while it was being typeset. We thank Jutta Schaper, MD, for taking care of the manuscript and preparing it for publication
{dagger}former Central Institute of Microbiology and Experimental Therapy Jena, Germany

Received 21 April 1993; revised 12 April 1994; .

Correspondence: E. G. Krause, MD, Max Delbrück Center of Molecular Medicine, Robert-Rössle Strasse 10, 13125 Berlin, Germany.

Abstract

The pathomechanisms of myocardial fibrosis are incompletely understood. Coronary microvessels (MV), interstitial reactions and focal myocardial lesions characterized by morphological signs of ischaemia were found in 39 spontaneous hypertensive rats (SHR) and 33 control rats aged 3, 13, 27, 52 and 78 weeks, using new morphological preparations and measuring methods. In the developing phase of spontaneous hypertension (SH) the numerical and area densities (developed for up to 13 weeks) of MV were lower than at 3 weeks and lower than control. The same was true for the fibrotic tissue density. However, all values were increased in the manifest phase of SH (27–78 weeks). The increase in interstitial tissue is topologically and causally related to pathological MV reactions that represent morphologically chronically increased contractions. Small MV that mostly elude detection with conventional staining methods are of particular importance. The first phase of manifest SH (27th–52nd week) is characterized by a generalized development of myocardial fibrosi the late phase (52nd–78th week) by a reinforced localized fibrosis that is attributable to the enhanced progression of focal ischaemic myocardial lesions. The septal region is not included in this phase. Thus, in the two phases of manifest SH, the pathomechanisms responsible for the development of myocardial fibrosis must be different.

Key Words: Coronary microvasculature • microvascular contraction • microvascular disease • long-term behaviour of microvasculature • myocardial ischaemia • hypertensive heart disease • experimental pathology • automated image analysis


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




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.