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[血管、血浆和细胞成分在调节血小板与内皮下相互作用中的作用更新]

[Update on the role of vascular, plasmatic and cellular components in the regulation of the interaction of platelets with the subendothelium].

作者信息

Ordinas A, Escolar G, Bastida E, Castillo R

机构信息

Servicio de Hemoterapia y Hemostasia, Hospital Clínic i Provincial, Barcelona.

出版信息

Sangre (Barc). 1990 Dec;35(6):425-32.

PMID:2087660
Abstract

The interaction of platelets (Plts) with subendothelium (SE) or with extracellular matrices (ECM) generated by endothelial cells was studied under flow conditions. The role of: a) platelet membrane glycoproteins (GPS) or subunits; b) plasma adhesive proteins such as von Willebrand factor (VWF) and fibronectin (Fn); and c) structural proteins of the SE such as laminin (Lm). Specific antibodies or purified proteins were added to the perfusates. GPS. Monoclonal antibodies (MoAb) directed against distinct epitopes of the GPIIb-IIIa affected in different manner the deposition of platelets. MoAb EDU3 decreased (p less than 0.01) the surface of the vessel covered by platelets (% CS) and increased the presence of platelets in contact (% C) with the SE. MoAb C17 did not modify the % CS but altered the morphological characteristics of the aggregates. A monoclonal antibody against GPIIb, decreased the % CS (p less than 0.01) without influencing % C; VWF. A linear progression of the % CS was observed for VWF levels ranging from 0.1 to 0.6 U/mL. A plateau was reached for concentrations of vWF above 0.6 U/mL; Fn. Perfusions in which blood was reconstituted with Fn-depleted plasma showed the cooperation of this protein facilitating Plt-Plt interaction. No statistical differences were observed in the % CS when ECM were incubated with a MoAb against Fn (3E3); Lm. The % CS decreased statistically (p less than 0.01) when SE or ECM were incubated with an antibody to Lm. These results show the critical role of vascular, plasmatic and cellular components in the maintenance of and adequate platelet function.

摘要

在流动条件下研究了血小板(Plts)与内皮下层(SE)或内皮细胞产生的细胞外基质(ECM)之间的相互作用。研究了以下因素的作用:a)血小板膜糖蛋白(GPS)或亚基;b)血浆粘附蛋白,如血管性血友病因子(VWF)和纤连蛋白(Fn);c)SE的结构蛋白,如层粘连蛋白(Lm)。将特异性抗体或纯化蛋白添加到灌注液中。GPS。针对GPIIb-IIIa不同表位的单克隆抗体(MoAb)以不同方式影响血小板的沉积。MoAb EDU3降低(p<0.01)了血小板覆盖的血管表面(%CS),并增加了与SE接触(%C)的血小板数量。MoAb C17未改变%CS,但改变了聚集体的形态特征。一种针对GPIIb的单克隆抗体降低了%CS(p<0.01),但不影响%C;VWF。对于VWF水平在0.1至0.6 U/mL范围内,观察到%CS呈线性增加。当vWF浓度高于0.6 U/mL时达到平台期;Fn。用缺乏Fn的血浆重构血液的灌注显示该蛋白促进血小板-血小板相互作用。当ECM与抗Fn单克隆抗体(3E3)孵育时,在%CS方面未观察到统计学差异;Lm。当SE或ECM与抗Lm抗体孵育时,%CS有统计学意义的降低(p<0.01)。这些结果表明血管、血浆和细胞成分在维持和保证血小板功能方面的关键作用。

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