Vander Velden P, Giles A R
Department of Pathology, Queen's University at Kingston, Ontario, Canada.
Br J Haematol. 1988 Nov;70(3):345-55. doi: 10.1111/j.1365-2141.1988.tb02493.x.
A standardized injury of the nail cuticle of normal, factor VII and factor VIII deficient dogs was used to study the evolution of the morphological changes occurring within the forming and formed haemostatic plug at the site of vascular injury. The morphological changes occurring were documented by light and transmission electron microscopy (TEM). Randomized measurements were made of the distances between adjacent platelets as a function of platelet interdigitation or compaction and the degree of dilatation of the open canalicular system (OCS) was used as an indicator of the degree of platelet activation. Fibrin deposition was noted both in terms of its location and the point in time at which it first appeared. TEM demonstrated major differences between the factor VIII deficient and the normal and factor VII deficient groups. In the normal animals the intermembrane distance showed noticeable changes with the platelets becoming tightly interdigitated at the time bleeding stopped. During the same period the OCS became dilated. These changes, which were not seen in the factor VIII deficient animals, continued until many platelets lost their intracellular content and became balloon cells or ghosts and fibrinous transformation became prominent. Although those events did occur in the factor VII deficient state, each was delayed and resulted in significant differences between the factor VII and normal animals suggesting that the extrinsic pathway may play an important role in initiating the changes noted. The results suggested that the generation of thrombin and/or factor Xa is essential to promote the initial stabilization of the platelet plug as well as initiating its subsequent consolidation by fibrinous transformation.
利用对正常犬、凝血因子VII缺乏犬和凝血因子VIII缺乏犬的甲皱襞进行标准化损伤，来研究血管损伤部位正在形成和已形成的止血栓内发生的形态学变化的演变过程。通过光学显微镜和透射电子显微镜（TEM）记录所发生的形态学变化。对相邻血小板之间的距离进行随机测量，作为血小板相互交错或压实的函数，并将开放小管系统（OCS）的扩张程度用作血小板活化程度的指标。记录纤维蛋白沉积的位置及其首次出现的时间点。TEM显示凝血因子VIII缺乏组与正常组和凝血因子VII缺乏组之间存在主要差异。在正常动物中，膜间距离显示出明显变化，出血停止时血小板紧密相互交错。在同一时期，OCS扩张。这些变化在凝血因子VIII缺乏的动物中未见到，一直持续到许多血小板失去细胞内成分并变成气球样细胞或幽灵样细胞，纤维蛋白转化变得明显。虽然这些事件在凝血因子VII缺乏状态下确实发生，但每一个都延迟了，导致凝血因子VII缺乏动物与正常动物之间存在显著差异，这表明外源性途径可能在引发所述变化中起重要作用。结果表明，凝血酶和/或因子Xa的产生对于促进血小板栓的初始稳定以及通过纤维蛋白转化启动其随后的巩固至关重要。
