Strukova S M, Umarova B A, Kulibali M
Vopr Med Khim. 1986 May-Jun;32(3):132-6.
Administration of heparin (2 un) into rats with depression of the anticoagulation system before treatment of the animals with alpha-thrombin (8 NIH un) inhibited the enzyme interaction with blood fibrinogen, which was manifested as a distinct decrease in content of soluble fibrin in blood as compared with its concentration evaluated after the treatment with thrombin. Heparin inhibited the reaction of thrombin with specific receptors in vascular walls. The effector response of the anticoagulation system, which is specific for interaction of free alpha-thrombin with the cell wall receptors, was not observed if thrombin was administered intravenously together with heparin. The patterns of the anticoagulation system were not altered after administration of the equimolar complex of DIP (diisopropyl phosphoryl)-alpha-thrombin and heparin, although free DIP-alpha-thrombin activated distinctly the anticoagulation system. The data obtained suggest that heparin, which inhibits partially the recognition site in thrombin molecule, impaired also the enzyme ability to bind to the specific receptors of vascular walls and therefore it impaired the distinct response of the anticoagulation system.
在用α-凝血酶(8 NIH单位)处理动物之前,给抗凝系统受抑制的大鼠注射肝素(2单位),可抑制该酶与血纤维蛋白原的相互作用,这表现为与用凝血酶处理后所评估的浓度相比,血液中可溶性纤维蛋白含量明显降低。肝素抑制凝血酶与血管壁中特异性受体的反应。如果将凝血酶与肝素静脉内一起给药,则未观察到抗凝系统对游离α-凝血酶与细胞壁受体相互作用所特有的效应反应。给予二异丙基磷酰基-α-凝血酶与肝素的等摩尔复合物后,抗凝系统的模式未改变,尽管游离的二异丙基磷酰基-α-凝血酶明显激活了抗凝系统。所获得的数据表明,肝素部分抑制凝血酶分子中的识别位点,也损害了该酶与血管壁特异性受体结合的能力,因此损害了抗凝系统的明显反应。