METHOD FOR MEASUREMENT OF CELL PROLIFERATION INHIBITING FACTOR IN HEART

广泛的纤维化在心肌病中是显著的。本研究的目的是研究遗传性心肌病仓鼠细胞外基质的主要成分之一--胶原的特性，并探讨其在心肌病发生发展中的作用。BIO53.58(5、11、22周)作为扩张型心肌病模型，BIO14.6(20、30周)作为肥厚型心肌病模型。以F1B为对照。BIO53.58和BIO14.6的胶原蛋白含量随着年龄的增长而增加。11周时BIO53.58和20周时BIO14.6的III型胶原显著增加。BIO14.6V型胶原在30周时明显减少。BIO53.58和BIO14.6中胶原的醋酸溶解度随纤维化进展而降低，而F1B中则不随纤维化进展而降低。可还原交联度在BIO53.58中呈递减趋势。BIO53.58和BIO14.6的组织学厚度较厚的胶原纤维增多。提示心肌病早期心肌细胞外基质具有未成熟组织的特点，富含III型胶原。在后期，基质类似于硬组织，其胶原主要是I型胶原，溶解度低。认为心脏内结合力较强的粗胶原纤维增多，除使心肌纤维变性、坏死外，还影响心脏的舒缩功能。

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 hereditarycardiomyopathic 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 cardiomyopahty. 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. Aceticacid 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. Histologicallythick 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 Icollagen and have low solubility. It is considered that the increase of the thick collagen fiber combined firmly in heart may affect the diastolicand the systolic function in addition to the loss of the cardiac muscle fiber by the deg eneration and the necrosis.