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Elevated levels of thrombin‐generating microparticles in stored red blood cells
Author(s) -
Gao Y.,
Lv L.,
Liu S.,
Ma G.,
Su Y.
Publication year - 2013
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/vox.12014
Subject(s) - thrombin generation , blood preservation , thrombin , andrology , red blood cell , chemistry , medicine , immunology , platelet , microbiology and biotechnology , biology
Background During storage, red blood cells ( RBC s) lose their membrane stability, leading to haemolysis and microparticle ( MP ) formation. The use of RBC s stored for more than 28 days has been associated with an increased incidence of deep vein thrombosis. However, the exact mechanism by which coagulation activation is enhanced in stored RBC s is still unknown. Objectives To investigate the relevant potential procoagulant activities of MP s and study the relative procoagulant factors for initiating the coagulation on MP s in stored RBC s. Study Design and Methods MPs were isolated from the plasma of RBC units stored in citrate–phosphate–dextrose–adenine. At seven storage time‐points (d0, d7, d14, d21, d28, d35 and d42), MP s were morphologically observed, quantified and analysed for tissue factor, factor XI ( FXI ) and their thrombin‐generating potential. Results MPs were observed using electron microscopy. The size of the MP s ranged from 0·272 μm to 0·973 μm in diameter. During the storage of RBC s in plastic bags, the MP concentration increased from 3389 ± 218/μl at day 0 to 61 586 ± 2237/μl at d42. Thrombin generation was dependent on the total number of MP s ( r = 0·987). Anti‐human FXI antibody inhibited thrombin concentrations by 50·3% compared with control plasma, whereas antitissue factor and antitissue factor pathway inhibitor failed to reduce thrombin concentrations. Conclusions Our study provides evidence that MP formation due to RBC storage might propagate coagulation not only by exposing phosphatidylserine, but also by initiating thrombin generation independently of tissue factor in a FXI ‐dependent manner.