title: Impact of red blood cell transfusion on platelet activation and aggregation in healthy volunteers: results of the TRANSFUSION study.
abstract: OBJECTIVE
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: 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.
authors.forename: Johanne
authors.initials: J
authors.lastname: Silvain
authors.forename: Ana
authors.initials: A
authors.lastname: Pena
authors.forename: Guillaume
authors.initials: G
authors.lastname: Cayla
authors.forename: David
authors.initials: D
authors.lastname: Brieger
authors.forename: Anne
authors.initials: A
authors.lastname: Bellemain-Appaix
authors.forename: Thomas
authors.initials: T
authors.lastname: Chastre
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Vignalou
authors.forename: Farzin
authors.initials: F
authors.lastname: Beygui
authors.forename: Olivier
authors.initials: O
authors.lastname: Barthelemy
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Collet
authors.forename: Gilles
authors.initials: G
authors.lastname: Montalescot
mesh_terms: D000328:Adult; D015815:Cell Adhesion Molecules / Q000378:metabolism; D017707:Erythrocyte Transfusion; D005260:Female; D005434:Flow Cytometry; D006400:Hematocrit / Q000379:methods; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism; D019007:P-Selectin / Q000378:metabolism; D010750:Phosphoproteins / Q000378:metabolism; D010766:Phosphorylation / Q000502:physiology; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D015815:Cell Adhesion Molecules; D006454:Hemoglobins; D008840:Microfilament Proteins; D019007:P-Selectin; D010750:Phosphoproteins; D010975:Platelet Aggregation Inhibitors; D000098662:Vasodilator-Stimulated Phosphoprotein