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Potentiation by red blood cells of shear-induced platelet aggregation:
relative importance of chemical and physical mechanisms
RC Reimers, SP Sutera and JH Joist
Evidence has been reported to indicate that red blood cells (RBCs) may
potentiate platelet adherence and platelet aggregation (PAG) in different
flow systems in vitro as well as hemostatic platelet plug formation in
response to vascular injury. In this study, we demonstrate that RBCs
enhance PAG induced by well-defined, low-intensity, uniform, laminar shear
stress. Potentiation by RBCs of shear-induced PAG was associated with
appreciable loss of adenine nucleotides from 14C- adenine-labeled RBCs, the
extent of which increased with increasing RBC concentration. The
concentrations of RBC-derived ADP measured in the medium after shear, as
determined by both high pressure liquid chromatography and the
luciferin/luciferase system, were within the range of concentrations of ADP
which may trigger PAG or potentiate PAG induced by low concentrations of
other platelet agonists in the aggregometer. To assess the relative
contribution of chemical (ADP) and physical (platelet surface transport)
mechanisms in the RBC-mediated potentiation of shear-induced PAG, aliquots
of citrated platelet-rich plasma (C-PRP) were exposed to shear stress in
the presence of untreated RBCs or RBCs exposed to an antihemolytic
concentration (5 mumol/L) of the membrane stabilizing agent, chlorpromazine
(CPZ). Potentiation of shear-induced PAG in the RBC-CPZ system was
significantly less than that in the untreated RBC system. However, CPZ-
induced reduction of PAG potentiation was associated with an increase
rather than a decrease in loss of adenine nucleotides from RBC.
Furthermore, shear-induced PAG in C-PRP as well as ADP- and collagen-
induced PAG in C-PRP in the aggregometer was significantly inhibited by 5
mumol/L CPZ, indicating that the observed reduced potentiation of
shear-induced PAG by RBCs in the presence of CPZ was due to a direct
inhibitory effect of the drug on platelets rather than a reduction of
shear-induced liberation of ADP from RBCs. When aliquots of C-PRP were
exposed to shear stress in the presence of RBCs completely depleted of ADP
by fixation in 1% glutaraldehyde, potentiation of PAG was approximately
half of that observed with intact RBCs. These findings indicate that both
RBC-derived ADP and RBC-mediated platelet surface transport are involved in
the potentiation by RBCs of PAG induced by laminar shear stress.
Volume 64,
Issue 6,
pp. 1200-1206,
12/01/1984
Copyright © 1984 by The American Society of Hematology
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