Shand R A, Butler K D, Davies J A, Menys V C, Wallis R B
Thromb Res. 1987 Mar 1;45(5):505-15. doi: 10.1016/0049-3848(87)90313-6.
Thrombus formation in the rabbit carotid artery has been studied kinetically in vivo using a minimally invasive technique utilising radioisotopes. Clamping of the carotid artery for 5 min resulted in the simultaneous accumulation of platelets and fibrin at the site of injury over the next 45 min. Under the electron microscope the response was seen to range from platelet monolayer adhesion to mural thrombus formation with fibrin deposition. In animals rendered thrombocytopenic, fibrin deposition was impaired during the first 15-20 minutes after injury. Basic coagulation times and fibrinogen concentration were within normal limits. In addition the injured vessels in these animals accumulated more radiolabelled albumin, but not erythrocytes, than injured vessels in control animals. The results may imply a role for platelets in the enhancement of fibrin deposition during the early part of the response to injury and in contributing to the maintenance of normal permeability following vessel injury.
利用放射性同位素的微创技术，在体内对家兔颈动脉血栓形成进行了动力学研究。夹闭颈动脉5分钟会导致在接下来的45分钟内血小板和纤维蛋白在损伤部位同时积聚。在电子显微镜下，可观察到从血小板单层黏附到伴有纤维蛋白沉积的壁血栓形成的一系列反应。在血小板减少的动物中，损伤后最初15 - 20分钟内纤维蛋白沉积受损。基础凝血时间和纤维蛋白原浓度在正常范围内。此外，与对照动物的损伤血管相比，这些动物的损伤血管积聚了更多的放射性标记白蛋白，但没有积聚红细胞。这些结果可能意味着血小板在损伤反应早期增强纤维蛋白沉积以及在维持血管损伤后正常通透性方面发挥作用。
