Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France.
Eur Heart J. 2010 Nov;31(22):2816-21. doi: 10.1093/eurheartj/ehq209. Epub 2010 Jun 29.
The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation.
In vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit.
Red blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y(12) activation pathway.
导致贫血急性冠脉综合征患者输注红细胞(RBC)后再次发生缺血性事件或死亡的潜在机制尚未完全阐明。本文旨在确定 RBC 输注是否会增加血小板的激活和聚集。
通过将取自输血袋的 RBC 添加到健康志愿者提供的新鲜全血中,进行体外输血(n = 45)。使用不同的 4 种激动剂进行透光比浊法测定,在体外输血前后评估残余血小板聚集(RPA)和最大血小板聚集(MPA)。使用流式细胞术测量 P-选择素表达和血管扩张刺激磷酸蛋白(VASP)血小板反应性指数(PRI)。为了控制血液浓缩的影响,使用志愿者的血小板缺乏血浆调整血细胞比容后,重复相同的实验。输注后,用 ADP 5 μM(57.7 ± 25 对 65.7 ± 24%;P = 0.03)或胶原 2 μg/mL(59.4 ± 28 对 69.7 ± 24%;P = 0.03)测量 RPA 时,血小板聚集增加。用花生四烯酸 1.25 mM 或肾上腺素 20 μM 时无显著差异,当考虑 MPA 时结果相似。通过输注增加血小板激活,如 20 μM ADP(12.2 ± 18 对 23.9 ± 18%;P = 0.002)或 50 μM ADP(15.4 ± 18.6 对 26.8 ± 21.2%;P = 0.004)诱导的 P-选择素表达升高以及 VASP PRI 升高(77.8 ± 6 对 81.9 ± 3%;P = 0.03)证实。这些作用均独立于血细胞比容。
在健康志愿者中,RBC 输注可增加体外血小板的激活和聚集。这种作用可能是通过 P2Y12 激活途径介导的。