Axial Dependence of Platelet‐Collagen Interactions in Flowing Blood: Upstream Thrombus Growth Impairs Downstream Platelet Adhesion
Axial Dependence of Platelet‐Collagen Interactions in Flowing Blood: Upstream Thrombus Growth Impairs Downstream Platelet Adhesion
复制标题
流动血液中血小板-胶原蛋白相互作用的轴向依赖性：上游血栓生长损害下游血小板粘附
DOI：
10.1161/01.atv.9.1.33
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
H. Baumgartner
中科院分区：
文献类型：
--
作者：
K. Sakariassen;H. Baumgartner
将血管内皮下和胶原表面暴露于流动的浓缩血液。在离暴露表面上游端不同轴向距离处研究血小板与这些表面的相互作用。在胶原表面上，血小板表面覆盖和血栓尺寸明显轴向减少。这种现象在200至2000 s-1的剪切速率下观察到，但在低剪切速率（<650 s-1）下最明显。在650 s-1剪切速率下灌注5分钟后，4.6 × 104个血小板沉积在胶原表面的最上游20 mm 2处，而在下游14 mm处，血小板沉积量为2.2 × 10 - 6/ 20 mm 2。血流边界层中von Wlllebrand因子和/或血栓反应蛋白的耗尽并不是造成这种情况的原因。胶原结合的von Wlllebrand因子增强了血小板的表面覆盖，而不影响轴向减量，而用血小板反应蛋白对胶原表面进行预处理则完全没有影响。然而，阿司匹林对血栓生长的部分抑制减少了轴向的减少，并且较少的血栓形成表面，如人和兔的内皮下，仅诱导少量小血栓，实际上在血小板粘附方面没有产生轴向差异。将剪切速率提高到2600 s-1也不会导致血小板-胶原粘附的轴向差异;但是，它确实会导致血栓尺寸的轴向增加。在向血液中加入抗人血小板凝血酶敏感蛋白抗体后，这种增加被中和。我们的数据是一致的，认为血小板表面相互作用是有限的血小板到达的表面在低于650 s-1的剪切速率。诱导上游血栓快速生长的表面可能会耗尽血小板的边界层，导致血小板粘附减少和血栓在更下游生长。在较高的剪切速率下，当血小板供应到表面不是限制因素时，从上游血栓释放的血小板反应蛋白似乎增强下游血栓生长和/或血栓稳定性。
Vascular subendothelium and collagenous surfaces were exposed to flowing cltrated blood. Platelet interactions with these surfaces were Investigated at various axial distances from the upstream end of the exposed surfaces. A pronounced axial decrease In surface coverage with platelets and in thrombus dimensions was encountered on collagenous surfaces. This phenomenon was observed at shear rates of 200 to 2000 s-1 but was most pronounced at low shear rates (<650 s-1). After 5 minutes of perfusion at a shear rate of 650 s−1 4.6 × 104 platelets were deposited on the most upstream 20 mm2 of the collagen surface, In contrast to 2.2 × 10−6 platelets/ 20 mm2 14 mm farther downstream. Depletion of von Wlllebrand factor and/or thrombospondin from the boundary layer of the blood flow was not responsible for this. Collagen-bound von Wlllebrand factor enhanced the surface coverage with platelets without affecting the axial decrement, while pretreatment of the collagen surface with thrombospondin had no effect at all. However, partial Inhibition of thrombus growth by aspirin reduced the axial decrements, and less thrombogenlc surfaces as human and rabbit subendothelium, which induced only a few small thrombi, produced virtually no axial differences In platelet adhesion. Raising the shear rate to 2600 s-1 also gave no axial differences In platelet-collagen adhesion; It did, however, give an axial Increase In thrombus dimensions. This Increase was neutralized after the addition of antibody against human platelet thrombospondin to the blood. Our data are consistent with the view that platelet-surface Interactions are limited by the arrival of platelets to the surface at shear rates below 650 s-1. Surfaces that Induce rapid-growing upstream thrombi may deplete the boundary layer for platelets, resulting In decreased platelet adhesion and thrombus growth farther downstream. At higher shear rates, when the platelet supply to the surface Is not a limiting factor, thrombospondin released from upstream thrombi appears to enhance downstream thrombus growth and/or thrombus stability.
影响因子：
3.1
作者：
T. Belval;J. Hellums;R. Solis
通讯作者：
T. Belval;J. Hellums;R. Solis