Nogami K, Kusachi S, Niiya K, Moritani H, Tsuji T
First Department of Internal Medicine, Okayama University Medical School, Japan.
Jpn Circ J. 1995 Sep;59(9):631-40. doi: 10.1253/jcj.59.631.
We examined changes in the distribution of extracellular matrix components in the myocardium of cardiomyopathic Syrian hamsters (BIO 14.6). Fibronectin, laminin, and type IV collagen, and type I and III collagens were immunohistochemically stained by the avidin-biotin-peroxidase complex method, using a polyclonal antibody for each component. Hearts obtained from 4 stages of BIO 14.6 cardiomyopathy were examined. Peri- and endomysial fibrosis increased as the disease progressed. Replacement and meshwork (perimysial fibrosis penetrating the intercellular space) fibrotic lesions appeared beginning in the 2nd stage, ie, the fibrotic and healing stage. All of the components examined, ie, fibronectin, laminin and type IV collagen, and type I and III collagens, were present in various fibrotic lesions and played a significant role in fibrotic changes throughout all of the stages of the disease. No primary deficit of any of these components was seen. An increased distribution of fibronectin was observed in both the enlarged peri-and endomysial spaces beginning in the initial stage, ie, the necrotic stage, when myocyte hypertrophy was inconspicuous, and distribution throughout the myocardium increased further as the disease progressed. Laminin and type IV collagen in the fibrotic lesions were not restricted to the myocyte membrane. Type III collagen was distributed in replacement and meshwork fibrotic lesions, and the extent of its distribution increased in proportion to that of type I collagen. The continuous increases in the distribution of fibronectin, laminin and type III collagen indicate that fibrotic changes occurred continuously in this model.(ABSTRACT TRUNCATED AT 250 WORDS)
