Gurewich V, Lipinski B, Hyde E
Thromb Haemost. 1976 Dec 31;36(3):605-14.
Fibrin formation from fibrin monomer (FM) complexes was studied in experimental animals utilizing a previously described technique for quantitating fibrin deposition. A uniform thrombin infusion was used to produce FM, fibrinolysis being inhibited by EACA. In vivo complex formation between FM and 125I-fibrinogen was demonstrated chromatographically. A direct correlation was found between blood fibrinogen concentration and fibrin deposition in organs. By contrast, an inverse correlation between fibrinogen concentration and both enzymatic or non-enzymatic fibrin formation was found in vitro. The mechanism by which fibrinogen potentiates FM precipitation in vivo could not be explained by coprecipitation of fibrinogen in the complex which could not be demonstrated. The inhibitory effect of HN2 on fibrin deposition despite the associated hyperfibrinogemia induced by this drug is believed to underscore the importance of leukocytes in certain types of fibrin deposition. A correlation between the leukocyte count and fibrin formation from FM was also found. It was concluded that the risk of intravascular fibrin deposition is increased by a raised fibrinogen level especially when accompanied by leukocytosis.
利用先前描述的定量纤维蛋白沉积的技术，在实验动物中研究了纤维蛋白单体（FM）复合物形成纤维蛋白的过程。采用均匀输注凝血酶来产生FM，用氨基己酸抑制纤维蛋白溶解。通过色谱法证明了FM与125I-纤维蛋白原在体内形成复合物。发现血液纤维蛋白原浓度与器官中纤维蛋白沉积之间存在直接相关性。相比之下，在体外发现纤维蛋白原浓度与酶促或非酶促纤维蛋白形成之间呈负相关。纤维蛋白原在体内增强FM沉淀的机制无法用复合物中纤维蛋白原的共沉淀来解释，因为并未证实存在这种共沉淀。尽管HN2会引起相关的高纤维蛋白原血症，但它对纤维蛋白沉积具有抑制作用，这被认为突出了白细胞在某些类型纤维蛋白沉积中的重要性。还发现白细胞计数与FM形成纤维蛋白之间存在相关性。得出的结论是，纤维蛋白原水平升高会增加血管内纤维蛋白沉积的风险，尤其是在伴有白细胞增多的情况下。
