血小板在胶原包被珠柱中的滞留机制。

M. Kaneko, O. Cuyun-Lira, T. Takafuta, K. Suzuki-Inoue, K. Satoh, K. Ohtsuki, M. Ohnishi, M. Arai, Y. Yatomi, Y. Ozaki
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引用次数: 1

摘要

尽管玻璃珠柱已被用于测量血小板粘附,但血小板与玻璃珠的相互作用是否代表生理过程仍未解决。为了获得更多的生理性血小板反应,最近开发了包被I型胶原蛋白的塑料珠来取代玻璃珠。在本研究中,我们分析了导致血小板滞留在胶原包被柱中的因素,并探讨了其可能的临床应用。我们用注射泵将柠檬酸全血样品以固定的速度泵入柱中,并通过测量通过柱前后的血小板计数来计算血小板保留率。来自健康供体的样本可高度重现的血小板保留率,在糖蛋白(GP) VI缺乏症患者中降低,但在III型血管性血液病患者中没有降低。抗gpiib /IIIa抗体和GRGDS肽明显抑制血小板保留,而抑制gpib -血管性血病因子或gpiia /IIIa -胶原相互作用无作用。各种抗血小板药物(包括抗凝血酶阿加曲班、前列环素、乙酰水杨酸和ADP清除剂磷酸肌酸/磷酸肌酸激酶)的作用数据支持该检测方法在临床应用中的有效性。我们的研究结果表明,GPVI和GPIIb/IIIa,而不是GPIb-von Willebrand因子的相互作用,主要参与血小板滞留。
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Mechanisms of platelet retention in the collagen-coated-bead column.
Although the glass-bead column has been used to measure platelet adhesion, whether platelet interaction with glass beads represents physiologic processes remains unsettled. In an attempt to obtain more physiologic platelet responses, plastic beads coated with type I collagen have been recently developed to replace glass beads. In this study, we analyzed the factors responsible for platelet retention in the collagen-coated-bead column and investigated its possible clinical applications. We pumped citrated whole-blood samples into columns at a fixed speed with an injection pump and calculated platelet-retention rates by measuring platelet counts before and after passage through the columns. The platelet-retention rates, which were highly reproducible with samples from healthy donors, were reduced in a patient with glycoprotein (GP) VI deficiency but not in patients with type III von Willebrand disease. Anti-GPIIb/IIIa antibody and GRGDS peptide markedly inhibited platelet retention, whereas inhibition of the GPIb-von Willebrand factor or GPIa/IIa-collagen interaction had no effect. Data on the effects of various antiplatelet agents (including the antithrombin agent argatroban, prostacyclin, acetylsalicylic acid, and the ADP scavenger creatine phosphate/creatine phosphokinase) support the usefulness of this assay method in clinical application. Our findings suggest that GPVI and GPIIb/IIIa but not the GPIb-von Willebrand factor interaction are mainly involved in platelet retention in this column.
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