Belousov Iu B, Sidorskiĭ A L, Abazova F I, Savenkov M P
Kardiologiia. 1977 Dec;17(12):94-8.
Using 125I-labelled fibrinogen the metabolism of this protein was studied in 29 patients with II-III stage congestive circulatory insufficiency due to ischemic heart disease and rheumatic heart diseases. It was established that with the progression of circulatory insufficiency fibrinogen half-life increased. The body content of total fibrinogen increased with the gradual intensification of circulatory insufficiency due to growth of the extravascular (noncirculating) fraction. The growth is associated with the intensified egress of circulating fibrinogen into the extravascular space (thrombus, tissue, etc.). The role of disseminated intravascular clotting and consumption coagulopathy in the pathogenesis of congestive circulatory failure is discussed.
使用125I标记的纤维蛋白原，对29例因缺血性心脏病和风湿性心脏病导致II - III期充血性循环功能不全的患者进行了该蛋白的代谢研究。结果表明，随着循环功能不全的进展，纤维蛋白原半衰期延长。由于血管外（非循环）部分增加，总纤维蛋白原的体内含量随着循环功能不全的逐渐加重而增加。这种增加与循环纤维蛋白原向血管外空间（血栓、组织等）的流出增加有关。文中讨论了弥散性血管内凝血和消耗性凝血病在充血性循环衰竭发病机制中的作用。
