PLATELET THROMBUS FORMATION ON COLLAGEN TYPE-I - A MODEL OF DEEP VESSEL INJURY - INFLUENCE OF BLOOD RHEOLOGY, VONWILLEBRAND-FACTOR, AND BLOOD-COAGULATION
PLATELET THROMBUS FORMATION ON COLLAGEN TYPE-I - A MODEL OF DEEP VESSEL INJURY - INFLUENCE OF BLOOD RHEOLOGY, VONWILLEBRAND-FACTOR, AND BLOOD-COAGULATION
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DOI：
10.1161/01.cir.78.6.1431
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发表时间：
1988-12-01
期刊：
影响因子：
37.8
通讯作者：
FUSTER, V
中科院分区：
文献类型：
--
作者：
BADIMON, L;BADIMON, JJ;FUSTER, V
I型胶原蛋白是动脉粥样硬化血管壁的主要成分，其暴露在深血管损伤中，例如在球囊血管成形术或斑块破裂中。将来自猪跟腱的I型胶原固定在置于体外回路（颈动脉至颈静脉）内的管状灌注室中。将材料暴露于来自正常猪（n = 13）、严重纯合血管性血友病因子（vWF）缺陷猪（vWF < 3%）（n = 6）和杂合vWF缺陷猪（vWF = 24%）（n = 2）的血液。血栓形成测定自体111 In-血小板标记和超微结构形态。将来自这些猪的肝素化血液和天然血液以212 - 3.380/sec的局部剪切速率灌注在基底上3和5分钟。对于暴露于非抗凝血液的I型胶原蛋白，在研究的所有暴露时间内，在不存在vWF的情况下，血栓形成在狭窄区域典型的高剪切率下显着减少，但在通畅的中等大小动脉典型的低剪切率下则没有显着减少。在肝素化和天然血液中均观察到由于vWF缺乏导致的血栓形成的类似抑制;然而，在肝素存在下血栓形成显著减少（p < 0.05），推测是由于在不存在纤维蛋白形成的情况下积聚的血小板缺乏稳定性。在杂合子型血管性血友病（vWD）中，中等水平的vWF支持血小板沉积，其程度与正常情况无显著差异。因此，在I型胶原上，凝血蛋白的活化和vWF的存在都显著促进血栓形成所必需的血小板-血小板相互作用。vWF的作用主要发生在高剪切条件下，典型的血管内血流在先进的狭窄病变的顶点，因此，这些研究结果可能表明，vWF的情况下，可能是保护对急性血栓形成的发展，在这些地区。
Collagen type I is a major component of atherosclerotic vessel wall that is exposed on deep vessel injury, such as in balloon angioplasty or plaque rupture. Collagen type I from pig Achilles tendon was mounted in a tubular perfusion chamber placed within an extracorporeal circuit (carotid artery to juglar vein). The material was exposed to blood from normal pigs (n = 13), severe homozygous von Willebrand factor (vWF)-deficient pigs (vWF < 3%) (n = 6), and heterozygous vWF-deficient pigs (vWF = 24%) (n = 2). Thrombus formation was measured by autologous 111In-platelet labeling and by ultrastructural morphology. Heparinized and native blood from these pigs was perfused over the substrate for 3 and 5 minutes at local shear rates from 212 to 3.380/sec. On collagen type I exposed to nonanticoagulated blood, for all exposure times studied, thrombus formation in the absence of vWF was significantly reduced at high shear rate typical of stenotic areas but not at low shear rate typical of unobstructed medium-size arteries. A similar inhibition in thrombus formation due to vWF deficiency was observed in both heparinized and native blood; however, thrombus formation was significantly more reduced (p < 0.05) in the presence of heparin, presumably due to the lack of stability of the accumulated platelets in the absence of fibrin formation. Intermediated levels of vWF, as in heterozygous von Willebrand''s disease (vWD), support platelet deposition to extents not significantly different from normal conditions. Therefore, on collagen type I, both the activation of blood coagulation proteins and the presence of vWF contribute significantly to the platelet-platelet interactions necessary for thrombus formation. The effect of vWF occurs primarily at high shear conditions typical intravascularly of flow at the apex of advanced stenotic lesions; thus, these findings may suggest that the absence of vWF may be protective against the development of acute thrombosis in these regions.