Sakariassen K S, Joss R, Muggli R, Kuhn H, Tschopp T B, Sage H, Baumgartner H R
F. Hoffmann-La Roche Ltd, Pharma Research/CVD, Basle, Switzerland.
Arteriosclerosis. 1990 Mar-Apr;10(2):276-84. doi: 10.1161/01.atv.10.2.276.
Exposure of type III collagen coats on plastic cover slips in parallel-plate perfusion chambers to flowing nonanticoagulated human blood resulted in deposition of platelets and fibrin. Blood was drawn directly from an antecubital vein by an occlusive roller pump over the collagen coats in chambers having flow slits of different dimensions, so that wall shear rates of 100, 650, and 2600 s-1 were obtained at 10 ml/min. Coagulation was minimally activated during the passage of blood from the vein to the chamber as shown by fibrinopeptide A levels of 3.7 ng/ml after 5-minute perfusions. The surface coverage with platelets increased from 18% at 100 s-1 to 59% at 2600 s-1, and the corresponding thrombus volumes increased from 2 to 22 microns 3/microns 2, respectively. This contrasted with the coverage with fibrin on collagen, which decreased from 28% at 100 s-1 to 9% at 2600 s-1. Fibrin deposits on the thrombi covered 6% of the surface irrespective of the shear rate, indicating that some of the deposited platelets accelerated the deposition of fibrin. The type III collagen preparation did not activate factor XII and did not possess tissue factor activity, indicating that the surface itself was not procoagulant. However, a correlation between deposited leukocytes and surface coverage with fibrin was observed (r = 0.78, p less than 0.01), suggesting a role for these cells in the deposition of fibrin. The data demonstrate that thrombogenesis is triggered by pure type III collagen, although the deposition of fibrin is not initiated by the collagen itself but presumably by deposited leukocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
将平行板灌注室中塑料盖玻片上的III型胶原涂层暴露于流动的非抗凝人血中会导致血小板和纤维蛋白沉积。通过闭塞式滚轴泵直接从前臂静脉抽取血液，使其流过具有不同尺寸流动缝隙的室中的胶原涂层，从而在流速为10 ml/min时获得100、650和2600 s-1的壁面剪切速率。如5分钟灌注后纤维蛋白肽A水平为3.7 ng/ml所示，血液从静脉进入室的过程中凝血被最小程度激活。血小板的表面覆盖率从100 s-1时的18%增加到2600 s-1时的59%，相应的血栓体积分别从2增加到22立方微米/平方微米。这与胶原上纤维蛋白的覆盖率形成对比，后者从100 s-1时的28%降至2600 s-1时的9%。血栓上的纤维蛋白沉积物覆盖了6%的表面，与剪切速率无关，表明一些沉积的血小板加速了纤维蛋白的沉积。III型胶原制剂未激活因子XII且不具有组织因子活性，表明表面本身不具有促凝性。然而，观察到沉积的白细胞与纤维蛋白的表面覆盖率之间存在相关性（r = 0.78，p < 0.01），提示这些细胞在纤维蛋白沉积中起作用。数据表明，虽然纤维蛋白的沉积不是由胶原本身引发的，可能是由沉积的白细胞引发的，但纯III型胶原可触发血栓形成。（摘要截短于250字）
