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Prepublished online as a Blood First Edition Paper on July 5, 2002; DOI 10.1182/blood-2002-03-0712.
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Blood, 15 November 2002, Vol. 100, No. 10, pp. 3797-3803
RED CELLS
Adhesion of normal erythrocytes at depressed venous shear rates
to activated neutrophils, activated platelets, and fibrin polymerized
from plasma
Mukul S. Goel and
Scott L. Diamond
From the Department of Chemical Engineering, Institute
for Medicine and Engineering, University of Pennsylvania, Philadelphia.
Deep vein thrombosis (DVT) is a low flow pathology often prevented
by vascular compression to increase blood movement. We report new
heterotypic adhesive interactions of normal erythrocytes operative at
low wall shear rates ( w) below 100 s 1.
Adhesion at w = 50 s 1 of washed red
blood cells (RBCs) to fibrinogen-adherent platelets was 4-fold less
(P < .005) than to collagen-adherent platelets (279 ± 105 RBC/mm2). This glycoprotein VI
(GPVI)-triggered adhesion was antagonized (> 80% reduction) by
soluble fibrinogen (3 mg/mL) and
ethylenediaminetetraacetic acid (EDTA). RBC-platelet
adhesion was reduced in half by antibodies against CD36 or GPIb, but
not by antibodies against GPIIb/IIIa, von Willebrand factor (VWF),
thrombospondin (TSP), P-selectin, 1, v,
or CD47. Adhesion of washed RBCs to fibrinogen-adherent neutrophils was
increased 6-fold in the presence of 20 µM N-formyl-Met-Leu-Phe to a
level of 67 RBCs per 100 neutrophils after 5 minutes at 50 s 1. RBC-neutrophil adhesion was diminished by
anti-CD11b (76%), anti-RBC Landsteiner-Wiener (LW) (ICAM4; 40%), or
by EDTA (> 80%), but not by soluble fibrinogen or antibodies against
CD11a, CD11c, CD36, TSP, 1, v, or CD47.
RBC adhesion to activated platelets and activated neutrophils was
prevented by wall shear stress above 1 dyne/cm2 (at 100 s 1). Whereas washed RBCs did not adhere to fibrin formed
from purified fibrinogen, adhesion was marked when pure fibrin was
precoated with TSP or when RBCs were perfused over fibrin formed from
recalcified plasma. Endothelial activation and unusually low flow may
be a setting prone to receptor-mediated RBC adhesion to adherent
neutrophils (or platelets/fibrin), all of which may contribute to DVT.

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