Shear-induced platelet aggregation can be mediated by vWF released from platelets, as well as by exogenous large or unusually large vWF multimers, requires adenosine diphosphate, and is resistant to aspirin
Shear-induced platelet aggregation can be mediated by vWF released from platelets, as well as by exogenous large or unusually large vWF multimers, requires adenosine diphosphate, and is resistant to aspirin
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剪切诱导的血小板聚集可由血小板释放的 vWF 以及外源性大或异常大的 vWF 多聚体介导，需要二磷酸腺苷，并且对阿司匹林具有耐药性
DOI：
10.1182/blood.v71.5.1366.bloodjournal7151366
复制
发表时间：
1988
期刊：
影响因子：
20.3
通讯作者：
J. Hellums
中科院分区：
文献类型：
--
作者：
J. Moake;N. Turner;N. Stathopoulos;L. Nolasco;J. Hellums
动脉粥样硬化或痉挛部分阻塞的动脉和小动脉的流体剪切应力可能超过正常的时间平均水平20达因/平方厘米。在体外，施加30至60达因/平方厘米的流体剪切应力30秒，血小板聚集发生。在这些剪切应力下，血小板外源性悬浮液中较大或异常大的血管性血友病因子（vWF）多聚体介导聚集。二磷酸腺苷（ADP）也是必需的，在这些实验中，它从受到剪切应力的血小板中释放出来。在120达因/平方厘米时，内源性血小板vWF多聚体的释放可以替代外源性大或异常大的vWF形式介导聚集。内源性释放的血小板vWF形式，以及外源性大或异常大的vWF多聚体，必须结合糖蛋白Ib和IIb/IIIa复合体才能产生聚集。剪切诱导聚集是血小板表面剪切应力改变的结果，而不是剪切效应对vWF多聚体的影响。它由大血浆型vWF多聚体、内源性释放血小板vWF形式或来自内皮细胞的异常大vWF多聚体介导，需要ADP，阿司匹林不明显抑制。这种类型的聚集在狭窄动脉血管内血小板血栓形成中可能是重要的，并且可能解释阿司匹林在动脉血栓形成中的治疗作用有限。
Fluid shear stress in arteries and arterioles partially obstructed by atherosclerosis or spasm may exceed the normal time-average level of 20 dyne/cm2. In vitro, at fluid shear stresses of 30 to 60 dyne/cm2 applied for 30 seconds, platelet aggregation occurs. At these shear stresses, either large or unusually large von Willebrand factor (vWF) multimers in the suspending fluid exogenous to the platelets mediates aggregation. Adenosine diphosphate (ADP) is also required and, in these experiments, was released from the platelets subjected to shear stress. At 120 dyne/cm2, the release of endogenous platelet vWF multimers can substitute for exogenous large or unusually large vWF forms in mediating aggregation. Endogenous released platelet vWF forms, as well as exogenous large or unusually large vWF multimers, must bind to both glycoproteins Ib and the IIb/IIIa complex to produce aggregation. Shear- induced aggregation is the result of shear stress alteration of platelet surfaces, rather than of shear effects on vWF multimers. It is mediated by either large plasma-type vWF multimers, endogenous released platelet vWF forms, or unusually large vWF multimers derived from endothelial cells, requires ADP, and is not inhibited significantly by aspirin. This type of aggregation may be important in platelet thrombus formation within narrowed arterial vessels, and may explain the limited therapeutic utility of aspirin in arterial thrombosis.
细胞质和可释放的 ADP 在层流剪切应力诱导的血小板聚集中的作用。
DOI：
--
发表时间：
1983
期刊：
The Journal of laboratory and clinical medicine
影响因子：
--
作者：
Moritz,MW;Reimers,RC;Baker,RK;Sutera,SP;Joist,JH
通讯作者：
Joist,JH
影响因子：
3.1
作者：
T. Belval;J. Hellums;R. Solis
通讯作者：
T. Belval;J. Hellums;R. Solis
冯维勒布兰德因子可以替代血浆纤维蛋白原参与 ADP 诱导的血小板聚集。
DOI：
--
发表时间：
1986
期刊：
Transactions of the Association of American Physicians
影响因子：
--
作者：
Timmons,S;Hawiger,J
通讯作者：
Hawiger,J