Keating Friederike K, Fung Mark K, Schneider David J
Department of Medicine and Pathology and Laboratory Medicine, University of Vermont, Burlington, VT 05401, USA.
Transfusion. 2008 Jun;48(6):1099-105. doi: 10.1111/j.1537-2995.2008.01692.x. Epub 2008 Mar 25.
Transfusion of red blood cell (RBC) preparations is independently associated with adverse clinical outcomes in patients with acute cardiovascular disease. This study was designed to define mechanisms potentially contributing.
The presence of platelets (PLTs), activated PLTs (PLTs expressing P-selectin), PLT-monocyte aggregates (PMAs), and PLT-neutrophil aggregates (PNAs) was determined in vitro with the use of flow cytometry in whole blood from healthy volunteers, in RBCs, and in whole blood after adding aliquots of RBCs. Both prestorage leukoreduced and nonleukoreduced RBCs were analyzed. Nonleukoreduced RBCs were subfractionated with the use of centrifugation and filtration to obtain a RBC-free and a cell-free fraction. Formation of PMAs and PNAs was determined in whole blood after the addition of aliquots of these subfractions.
Nonleukoreduced RBCs contained 50 +/- 18 percent of the PLTs found in whole blood from healthy volunteers, and 43 +/- 16 percent of the PLTs were activated. Leukoreduced RBCs contained few PLTs (0.2 +/- 0.1% of volunteer blood). The majority (>60%) of white blood cells (WBCs) in nonleukoreduced RBCs were associated with PLTs. The formation of PMAs and PNAs in whole blood was increased approximately fivefold after addition of nonleukoreduced-RBCs (p < 0.0001) and by less than twofold with leukoreduced RBCs (p = 0.01). Addition of the essentially cell-free fraction of nonleukoreduced RBCs did not increase the formation of PNA or PMA in whole blood significantly.
RBC preparations, particularly nonleukoreduced RBCs, contain activated PLTs and PLT-WBC aggregates and induce formation of PLT-WBC aggregates. This may be one mechanism contributing to adverse outcomes linked to transfusions in patients with cardiovascular disease.
输注红细胞（RBC）制剂与急性心血管疾病患者的不良临床结局独立相关。本研究旨在确定可能起作用的机制。
使用流式细胞术在体外测定健康志愿者全血、RBC以及添加等分RBC后的全血中血小板（PLT）、活化血小板（表达P-选择素的PLT）、血小板-单核细胞聚集体（PMA）和血小板-中性粒细胞聚集体（PNA）的存在情况。对储存前白细胞滤除和未滤除的RBC均进行了分析。未白细胞滤除的RBC通过离心和过滤进行亚分级，以获得无RBC部分和无细胞部分。添加这些亚分级部分的等分试样后，在全血中测定PMA和PNA的形成情况。
未白细胞滤除的RBC中所含PLT占健康志愿者全血中PLT的50±18%，且43±16%的PLT被激活。白细胞滤除的RBC中PLT很少（占志愿者血液的0.2±0.1%）。未白细胞滤除的RBC中大多数（>60%）白细胞（WBC）与PLT相关。添加未白细胞滤除的RBC后，全血中PMA和PNA的形成增加约五倍（p<0.0001），而添加白细胞滤除的RBC后增加不到两倍（p = 0.01）。添加未白细胞滤除的RBC的基本无细胞部分不会显著增加全血中PNA或PMA的形成。
RBC制剂，尤其是未白细胞滤除的RBC，含有活化的PLT和PLT-WBC聚集体，并诱导PLT-WBC聚集体的形成。这可能是导致心血管疾病患者输血相关不良结局的一种机制。
