[An investigation of the collagen in cardiomyopathic hamsters].
Extensive fibrosis is remarkable in cardiomyopathy. The purpose of this study is to characterize the collagen, one of the chief elements of the extracellular matrix of hereditary cardiomyopathic hamsters, and to examine the participation of the collagen in the occurrence and the progression of the cardiomyopathy. BIO53.58 (5, 11, 22 weeks) was used as the model of the dilated cardiomyopathy and BIO14.6 (20, 30 weeks) was used as the model of the hypertrophic cardiomyopathy F1b was used as the control. The collagen content was almost constant at any age in F1b, but increased with aging in BIO53.58 and BIO14.6. Type III collagen increased significantly in BIO53.58 at 11 weeks and BIO14.6 at 20 weeks. Type V collagen decreased significantly in BIO14.6 at 30 weeks. Acetic acid solubility of collagen decreased in BIO53.58 and BIO14.6 with the progression of the fibrosis, but not in F1b. Reducible crosslinks showed the tendency to decrease in BIO53.58 progressively. Histologically thick collagen fiber increased in BIO53.58 and BIO14.6. These findings indicate that in the early phase of the cardiomyopathy the extracellular matrix of the myocardium has characteristics that of the immature tissues which are rich in type III collagen. In later phase, the matrix resembles that of hard tissues whose collagen is mainly of type I collagen and have low solubility. It is considered that the increase of the thick collagen fiber combined firmly in heart may affect the diastolic and the systolic function in addition to the loss of the cardiac muscle fiber by the degeneration and the necrosis.
Okada
H
H
Hokkaido University School of Medicine, Sapporo, Japan.
D000818:Animals; D009202:Cardiomyopathies / Q000473:pathology / Q000503:physiopathology*; D003094:Collagen / Q000032:analysis / Q000502:physiology*; D006224:Cricetinae; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000502:physiology*; D008297:Male; D008647:Mesocricetus
D003094:Collagen