Bertaggia Calderara Debora, Crettaz David, Aliotta Alessandro, Barelli Stefano, Tissot Jean-Daniel, Prudent Michel, Alberio Lorenzo
Division of Hematology and Central Hematology Laboratory, CHUV, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Laboratoire de Recherche sur les Produits Sanguins, Transfusion Interrégionale CRS, Epalinges, Switzerland.
Transfusion. 2018 Oct;58(10):2395-2406. doi: 10.1111/trf.14883. Epub 2018 Sep 19.
Collagen- and thrombin-activated (COAT) platelets (PLTs), generated by dual-agonist stimulation with collagen and thrombin (THR), enhance THR generation at the site of vessel wall injury. There is evidence that higher amounts of procoagulant COAT PLTs are associated with stroke, while a decreased ability to generate them is associated with bleeding diathesis. Our aim was to study PLT functions, particularly the ability to generate COAT PLTs, in PLT concentrates (PCs) from buffy coat. Thus, we investigated the effect of processing, pathogen inactivation treatment (amotosalen-UVA), and PC storage.
Two PCs from five donors each were pooled and split in two bags; one of them was pathogen inactivated and the other one was left untreated (n = 5). Flow cytometric analyses were performed immediately after PC preparation (Day 1) and thereafter on Days 2, 5, 7, and 9 in treated and untreated PCs to measure the reactivity of PLTs (CD62P and PAC-1), the content and secretion of dense granule after stimulation with different agonists, and the percentage of COAT PLTs after dual stimulation with convulxin (agonist of the collagen receptor GPVI) and THR.
Preparation of PCs resulted in a significant decrease of COAT PLTs and in an impaired response to adenosine 5'-diphosphate sodium (ADP). Storage further decreased ADP response. Minor differences were observed between untreated or amotosalen-UVA-treated PCs.
Preparation of PCs from buffy coats decreased the ability to generate COAT PLTs and impaired PLT response to ADP.
胶原蛋白和凝血酶激活（COAT）的血小板（PLT）由胶原蛋白和凝血酶（THR）双重激动剂刺激产生，可增强血管壁损伤部位的THR生成。有证据表明，较高数量的促凝血COAT PLT与中风有关，而生成它们的能力下降与出血素质有关。我们的目的是研究来自血沉棕黄层的血小板浓缩物（PC）中PLT的功能，特别是生成COAT PLT的能力。因此，我们研究了处理、病原体灭活处理（氨甲环酸-紫外线A）和PC储存的影响。
将来自五个供体的两台PC合并并分成两袋；其中一袋进行病原体灭活，另一袋不进行处理（n = 5）。在PC制备后立即（第1天）以及之后的第2、5、7和9天，对处理过和未处理过的PC进行流式细胞术分析，以测量PLT的反应性（CD62P和PAC-1）、用不同激动剂刺激后致密颗粒的含量和分泌，以及用convulxin（胶原蛋白受体GPVI的激动剂）和THR双重刺激后COAT PLT的百分比。
PC的制备导致COAT PLT显著减少，并且对5'-二磷酸腺苷钠（ADP）的反应受损。储存进一步降低了ADP反应。在未处理或氨甲环酸-紫外线A处理的PC之间观察到微小差异。
从血沉棕黄层制备PC降低了生成COAT PLT的能力，并损害了PLT对ADP的反应。
