help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cohen-Gould, L.
Right arrow Articles by Factor, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cohen-Gould, L.
Right arrow Articles by Factor, S. M.

American Journal of Pathology, Vol 127, 327-334, Copyright © 1987 by American Society for Investigative Pathology

REGULAR ARTICLES

Intrinsic connective tissue abnormalities in the heart muscle of cardiomyopathic Syrian hamsters

L Cohen-Gould, TF Robinson and SM Factor

Significant connective tissue abnormalities occurring in hearts of cardiomyopathic Syrian hamsters are reported. These abnormalities include a pronounced loss of the intrinsic connective tissue skeletal framework around foci of myocytolytic necrosis within the non-necrotic myocardium. These changes were demonstrated by a silver impregnation technique, and they were confirmed by scanning electron microscopy. Quantitation demonstrated more than a twofold increase in the area of ventricular wall affected by pathologic changes, when the connective tissue alterations were included with the myocardial necrosis. In addition, the authors also observed focal, thick "tethering" connective tissue fibers at the termini of necrotic lesions, seemingly connecting them to normal muscle. These connective tissue abnormalities may contribute to the progressive loss of ventricular function that occurs in this model of cardiomyopathy. They may permit greater wall thinning than would occur with focal necrosis alone, and they may increase focal mural stiffness in the tethered regions. Further investigation of the pathogenesis of these changes and their mechanical significance is indicated.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
P. W. M. Fedak, S. M. Altamentova, R. D. Weisel, N. Nili, N. Ohno, S. Verma, T.-Y. J. Lee, C. Kiani, D. A. G. Mickle, B. H. Strauss, et al.
Matrix remodeling in experimental and human heart failure: a possible regulatory role for TIMP-3
Am J Physiol Heart Circ Physiol, February 1, 2003; 284(2): H626 - H634.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
I. M.C. Dixon, J. Hao, N. L. Reid, and J. C. Roth
Effect of chronic AT1 receptor blockade on cardiac Smad overexpression in hereditary cardiomyopathic hamsters
Cardiovasc Res, May 1, 2000; 46(2): 286 - 297.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1987 by the American Society for Investigative Pathology.