Tippe A, Müller-Mohnssen H
GSF, Dept. of Physiology, Neuherberg, Germany.
Thromb Res. 1993 Dec 1;72(5):379-88. doi: 10.1016/0049-3848(93)90238-j.
Fibrin thrombus formation, in vivo and in vitro, preferentially occurs in regions of retarded, recirculating flow which promote local variations of the distribution of blood components, e.g. thrombin, and shear rates. To better understand the effects of shear forces on the thrombin induced fibrin coagulation process the time course of fibrin formation in a fibrinogen/thrombin solution was studied for different shear rates gamma (0 s-1 < or = gamma < or = 500 s-1) and thrombin concentrations cthr (0.1 units/ml < or = cthr < or = 1.0 units/ml). The clotting curves at zero shear and the shear induced alterations of these curves could essentially be described in terms of a reaction kinetics defined by two rate coefficients k1, k2 which can be attributed to fibrinogen cleavage by thrombin and fibrin polymerisation, respectively. For cthr > approximately 0.5 units/ml and gamma > approximately 15 s-1 an additional mechanism, presumably fibrin breakage, had to be assumed. The rate coefficient k2 was markedly more affected by cthr and shear forces then was k1. The results fit well to the growth kinetics of fibrin thrombi formed in glass models of an arterial branching.
在体内和体外,纤维蛋白血栓的形成优先发生在血流缓慢、循环的区域,这些区域会促进血液成分(如凝血酶)分布和剪切速率的局部变化。为了更好地理解剪切力对凝血酶诱导的纤维蛋白凝固过程的影响,研究了在不同剪切速率γ(0 s-1≤γ≤500 s-1)和凝血酶浓度cthr(0.1单位/毫升≤cthr≤1.0单位/毫升)下,纤维蛋白原/凝血酶溶液中纤维蛋白形成的时间进程。零剪切力下的凝血曲线以及这些曲线的剪切诱导变化基本上可以用由两个速率系数k1、k2定义的反应动力学来描述,这两个系数分别归因于凝血酶对纤维蛋白原的裂解和纤维蛋白聚合。对于cthr>约0.5单位/毫升且γ>约15 s-1的情况,必须假定存在另一种机制,可能是纤维蛋白断裂。速率系数k2受cthr和剪切力的影响明显大于k1。这些结果与动脉分支玻璃模型中形成的纤维蛋白血栓的生长动力学非常吻合。