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Examination of the roles of glycoprotein Ib and glycoprotein IIb/IIIa in
platelet deposition on an artificial surface using clinical antiplatelet
agents and monoclonal antibody blockade
RA Sheppeck, M Bentz, C Dickson, S Hribar, J White, J Janosky, SA Berceli, HS Borovetz and PC Johnson
Department of Surgery, University of Pittsburgh School of Medicine, PA.
The mechanism of platelet thrombus growth on an artificial surface is
incompletely understood. While glycoprotein (GP)Ib and GPIIb/IIIa are
required for normal attachment and thrombus formation on subendothelium,
their roles in platelet deposition to artificial surfaces remain unclear.
Using selected platelet inhibitors (aspirin [ASA], low molecular weight
dextran, monoclonal antibodies 10E5 [v GPIIb/IIIa], and 6D1 [GPIb]) we
examined the mechanism of platelet deposition to polyethylene (PE) surfaces
under steady laminar and oscillatory flow conditions. Polyethylene-100
(PE-100) tubes (0.86 mm internal diameter) were perfused under steady
laminar flow with citrated human whole blood reconstituted with
111indium-labeled platelets at 312 seconds-1 shear rate in the presence and
absence of platelet inhibitors. The effect of oscillatory flow on platelet
deposition was examined in a microwell system using 3/16-inch diameter
discs of National Heart, Lung, and Blood Institute primary reference PE as
the test surface. ASA and dextran did not significantly (P greater than
.05) inhibit platelet deposition in laminar flow (not tested in
oscillatory). Antibody 10E5 was a potent inhibitor (laminar less than 1%, P
less than .0001, oscillatory less than 1.6%, P less than .01) of platelet
deposition in both systems, and in this case, true adhesion (first attached
layer) was blocked. Antibody 6D1 unexpectedly inhibited 70% of platelet
deposition (P less than .01) in steady laminar flow and 56.5% in
oscillatory flow (P less than .01). Scanning electron microscopy
demonstrated platelets atop platelets in the controls, rare platelets in
the 10E5 group, and a patchy monolayer of platelets in the 6D1 group.
Transmission electron microscopy of cross-sections confirmed these
observations. We conclude that the adhesion of the first platelet layer to
an artificial surface requires GPIIb/IIIa. The data also suggest that GPIb
is required for the development of the second layer in vertical platelet
thrombus growth.
Volume 78,
Issue 3,
pp. 673-680,
08/01/1991
Copyright © 1991 by The American Society of Hematology
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