一个灌注室的发展,以调查血栓形成和剪切剖面在流动的原生人类血液在明确的狭窄。

R M Barstad, H E Roald, Y Cui, V T Turitto, K S Sakariassen
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引用次数: 73

摘要

导致中风、心肌梗死和/或猝死的突发事件可能与狭窄斑块破裂或表面受损部位的壁栓形成有关。动脉粥样硬化斑块的流体动力学特性可能与血栓形成有关,已经在斑块破裂过程和血小板血栓形成过程的各种模型系统中得到了描述。一般来说,局部流体动力条件是复杂的,并且与明确定义的层流系统的流动表现出很大的变化。然而,没有研究试图量化狭窄相关干扰对人体血液血栓形成的影响,并将其与局部流体动力学进行比较。我们开发了一种平行板灌注室装置,其中在偏心狭窄的“顶点”测量血栓形成,并将这些测量值与计算机模拟获得的局部流体动力学值相关联。狭窄程度(血流通道横截面积减少)分别为60%,80%和89%,对应于“顶点”壁剪切率分别为2600,10,500和32,000 sec-1。狭窄区近端和远端层流区管壁剪切速率为420秒-1。狭窄的表面是纯化的III型胶原原纤维,这些原纤维暴露于流动的非抗凝人类血液中,这些血液是通过放置在灌注室远端的泵直接从肘前静脉抽取的。由此产生的血液-胶原蛋白相互作用通过光学显微镜定量使用形态测量图像分析技术。在所有研究条件下,“尖端”血小板血栓形成广泛。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A perfusion chamber developed to investigate thrombus formation and shear profiles in flowing native human blood at the apex of well-defined stenoses.

The precipitating event leading to stroke, myocardial infarction, and/or sudden death may be related to the formation of mural thrombus at the site of a ruptured or superficially damaged stenotic plaque. The fluid dynamic properties at atherosclerotic plaques that may be implicated in this thrombus formation have been described in a wide variety of model systems in both the process of plaque rupture and the growth of platelet thrombi. In general, the local fluid dynamic conditions are complex and show major variations from flow in well-defined laminar flow systems. However, no studies have attempted to quantify the effect of stenosis-related disturbances on thrombus formation in native human blood and to compare them with the local fluid dynamics. We developed a parallel-plate perfusion chamber device in which thrombus formation is measured at the "apex" of eccentric stenoses and have correlated such measurements with values of the local fluid dynamics obtained by computer simulation. The extent of stenoses (reduction in the cross-sectional area of the blood flow channel) was 60%, 80%, and 89%, corresponding to "apex" wall shear rates of 2600, 10,500, and 32,000 sec-1, respectively. The wall shear rate in the laminar flow region proximal and distal to the stenoses was 420 sec-1. The surface of the stenosis was purified collagen type III fibrils that were exposed to flowing nonanticoagulated human blood drawn directly from an antecubital vein by a pump placed distally to the perfusion chamber. The resulting blood-collagen interactions were quantified by light microscopy by using a morphometric image analysis technique. Under all conditions studied, platelet thrombus formation at the "apex" was extensive.(ABSTRACT TRUNCATED AT 250 WORDS)

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