Shear-induced platelet activation and platelet microparticle formation at blood flow conditions as in arteries with a severe stenosis
Shear-induced platelet activation and platelet microparticle formation at blood flow conditions as in arteries with a severe stenosis
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DOI：
10.1161/01.atv.17.4.646
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发表时间：
1997-04-01
影响因子：
8.7
通讯作者：
Sakariassen, KS
中科院分区：
文献类型：
--
作者：
Holme, PA;Orvim, U;Sakariassen, KS
在本研究中，我们研究了在不同暴露时间的高动脉切应力或狭窄引起的切应力突然增加是否会影响天然人血液中的血小板活化和血小板微粒形成。我们使用了一个平行板灌注室装置，通过该装置，用泵直接从肘前静脉通过灌注室的流动通道以420、2600和10 500 s（-1）的壁剪切速率抽取未抗凝的人血（10 mL/min）。在另一组实验中，偏心狭窄被引入到流动通道中。在相同的流速下，狭窄顶点处的壁剪切率保持在2600或10 500 s（-1）。这些狭窄上游和下游的壁剪切速率为420 s（-1）。420 s（-1）的剪切率在健康小冠状动脉中遇到的剪切率范围内，而2600和10 500 s（-1）的剪切率则代表不同程度狭窄病变的血管。将血液暴露于这些剪切速率下0.075 - 3.045秒。血小板活化通过FITC标记的单克隆抗体（MAb）PAC-1和FITC标记的膜联蛋白V的氨基磷脂转位评估为活化的糖蛋白（GP）IIb/IIIa。微粒形成通过针对GP IIIa的FITC标记的MAb Y2/51定量。仅在10 500 s（-1）时观察到显著的血小板活化和微粒形成（P
In the present study, we investigated whether high arterial shear stresses at various exposure times or a sudden increase in shear stress introduced by a stenosis affect platelet activation and platelet microparticle formation in native human blood. We used a parallel-plate perfusion chamber device through which nonanticoagulated human blood was drawn (10 mL/min) by a pump directly from an antecubital vein through the flow channel of a perfusion chamber at wall shear rates of 420, 2600, and 10 500 s(-1). In another set of experiments, an eccentric stenosis was introduced into the flow channel. Wall shear rates of 2600 or 10 500 s(-1) at the stenosis apex were maintained at the same flow rate. The wall shear rate upstream and downstream of these stenoses was 420 s(-1). A shear rate of 420 s(-1) is within the range of those encountered in healthy small coronary arteries, whereas those of 2600 and 10 500 s(-1) are representative for vessels with various degrees of stenotic lesions. The blood was exposed to these shear rates for periods varying from 0.075 to 3.045 seconds. Platelet activation was assessed as activated glycoprotein (GP) IIb/IIIa by FITC-labeled monoclonal antibody (MAb) PAC-1 and aminophospholipid translocation by FITC-labeled annexin V. Microparticle formation was quantified by FITC-labeled MAb Y2/51 directed against GP IIIa. Significant platelet activation and formation of microparticles were observed at 10 500 s(-1) only (P