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。本研究的目的是对遗传性心肌病仓鼠细胞外基质的主要成分之一胶原蛋白进行表征，并探讨胶原蛋白在心肌病发生发展中的作用。采用BIO53.58（5、11、22周）作为扩张型心肌病模型，采用BIO14.6（20、30周）作为肥厚型心肌病模型。以F1b为对照。在F1b中，胶原含量在任何年龄几乎不变，但在BIO53.58和BIO14.6中，胶原含量随着年龄的增长而增加。11周时BIO53.58和20周时BIO14.6型胶原蛋白显著升高。30周时，BIO14.6的V型胶原蛋白明显减少。在BIO53.58和BIO14.6中，胶原的醋酸溶解度随着纤维化的进展而下降，但在F1b中没有。可还原交联在BIO53.58中呈逐渐减少的趋势。在BIO53.58和BIO14.6中，胶原纤维厚度增加。这些结果表明，在心肌病早期，心肌细胞外基质具有富含III型胶原的未成熟组织的特征。在后期，基质类似于硬组织，胶原主要为胶原型，溶解度低。认为除了心肌纤维因变性和坏死而丧失外，在心脏内紧密结合的厚胶原纤维的增加也可能影响心脏舒张和收缩功能。

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.