Johnstone I B
Can J Comp Med. 1983 Apr;47(2):157-62.
Thrombokinetograms are graphic depictions of the optical changes occurring in plasma during the clotting process and provide information, not only on the time required for clotting to begin, but also on the way in which the clot forms. We studied thrombokinetic profiles in plasmas from normal dogs, and dogs with varying degrees of factor VIII deficiency. Clotting was induced through intrinsic, extrinsic and common coagulation pathways [activated partial thromboplastin time, prothrombin time and thrombin time, respectively]. The thrombokinetograms for the various clotting tests were qualitatively similar in normal canine plasmas. After activation of the clotting system there was a period in which no change in optical density occurred. This period was represented by the left base line and corresponded to the duration of the clotting time. When fibrin production commenced there was a rapid increase in the rate of optical density change (DeltaOD) to a maximum (V(max)DeltaOD) in time t(1). This was followed by a more gradual reduction in DeltaOD in time t(2). The activated partial thromboplastin time thrombokinetograms for von Willebrand's disease plasmas were characterized by a reduced V(max)DeltaOD and prolonged t(1). In severe hemophilic plasma [factor VIII coagulant (F VIII:C)<1% of normal] there was a very slow increase in DeltaOD following a prolonged left baseline. The V(max)DeltaOD, t(1) and t(2) could not be determined since a peak was not attained in one minute. The prothrombin and thrombin time thrombokinetograms for von Willebrand's disease plasmas were normal. The prothrombin time thrombokinetogram for hemophilic plasma had a 2X normal V(max)DeltaOD possibly related to the relatively high fibrinogen concentration of this plasma compared to the normal. Changes in thrombokinetogram profiles may be of value in studying mild to moderate clotting factor deficiencies particularly where the clotting times are not markedly prolonged.
血栓动图是凝血过程中血浆发生的光学变化的图形描绘,它不仅能提供凝血开始所需的时间信息,还能提供血栓形成方式的信息。我们研究了正常犬和不同程度因子VIII缺乏犬血浆的血栓动力学特征。通过内源性、外源性和共同凝血途径(分别为活化部分凝血活酶时间、凝血酶原时间和凝血酶时间)诱导凝血。正常犬血浆中各种凝血试验的血栓动图在质量上相似。凝血系统激活后,有一段时间光密度没有变化。这段时间由左基线表示,对应于凝血时间的持续时间。当纤维蛋白产生开始时,光密度变化率(DeltaOD)迅速增加,在时间t(1)达到最大值(V(max)DeltaOD)。随后,DeltaOD在时间t(2)逐渐降低。血管性血友病血浆的活化部分凝血活酶时间血栓动图的特征是V(max)DeltaOD降低和t(1)延长。在严重血友病血浆[因子VIII凝血剂(F VIII:C)<正常的1%]中,左基线延长后DeltaOD增加非常缓慢。由于一分钟内未达到峰值,因此无法确定V(max)DeltaOD、t(1)和t(2)。血管性血友病血浆的凝血酶原时间和凝血酶时间血栓动图正常。血友病血浆的凝血酶原时间血栓动图的V(max)DeltaOD是正常的2倍,这可能与该血浆中纤维蛋白原浓度相对较高有关。血栓动图特征的变化在研究轻度至中度凝血因子缺乏时可能有价值,特别是在凝血时间没有明显延长的情况下。