Thomas D P, Merton R E, Wood R D, Hockley D J
Br J Haematol. 1985 Mar;59(3):449-57. doi: 10.1111/j.1365-2141.1985.tb07332.x.
The relative importance of stasis, vessel wall damage and hypercoagulability in the pathogenesis of venous thrombosis remains disputed. While the combination of local vascular stasis and systemic hypercoagulability can be shown to produce experimental thrombi within a few minutes, it has been claimed that vessel wall damage is also a necessary component of venous thrombogenesis. In this experimental study, mechanical crushing of the jugular veins produced patchy areas of denuded endothelium, with underlying vessel wall oedema, as seen by ultrastructural examination. While the exposed subendothelium became covered with activated platelets following restored blood flow, there was no fibrin formation after 5 min. When blood flow was restored for 60 min following the crush injury, white cells could be seen adhering to and migrating through the vessel wall, although there was still no visible fibrin. The addition of venous stasis for 20 min did not lead to the formation of stasis thrombi in association with the damaged areas. The present experiments demonstrate that, far from there being subtle endothelial damage contributing to acute venous thrombosis, even readily demonstrable damage is a poor stimulus to fibrin formation at local sites of vessel wall injury.
在静脉血栓形成的发病机制中，血流淤滞、血管壁损伤和高凝状态的相对重要性仍存在争议。虽然局部血管淤滞和全身高凝状态相结合可在几分钟内产生实验性血栓，但有人认为血管壁损伤也是静脉血栓形成的必要组成部分。在本实验研究中，通过超微结构检查可见，颈静脉机械挤压产生了内皮剥脱的片状区域，并伴有血管壁水肿。尽管血流恢复后暴露的内皮下层被活化的血小板覆盖，但5分钟后仍无纤维蛋白形成。挤压伤后血流恢复60分钟时，可见白细胞黏附并穿过血管壁，尽管仍无可见纤维蛋白。增加20分钟的静脉淤滞并未导致与损伤区域相关的淤滞性血栓形成。目前的实验表明，急性静脉血栓形成并非由细微的内皮损伤所致，即使是易于证实的损伤对血管壁损伤局部的纤维蛋白形成也缺乏刺激作用。
