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Shear-induced platelet aggregation can be mediated by vWF released from
platelets, as well as by exogenous large or unusually large vWF multimers,
requires adenosine diphosphate, and is resistant to aspirin
JL Moake, NA Turner, NA Stathopoulos, L Nolasco and JD Hellums
Biomedical Engineering Laboratory, Rice University, Houston, TX 77251.
Fluid shear stress in arteries and arterioles partially obstructed by
atherosclerosis or spasm may exceed the normal time-average level of 20
dyne/cm2. In vitro, at fluid shear stresses of 30 to 60 dyne/cm2 applied
for 30 seconds, platelet aggregation occurs. At these shear stresses,
either large or unusually large von Willebrand factor (vWF) multimers in
the suspending fluid exogenous to the platelets mediates aggregation.
Adenosine diphosphate (ADP) is also required and, in these experiments, was
released from the platelets subjected to shear stress. At 120 dyne/cm2, the
release of endogenous platelet vWF multimers can substitute for exogenous
large or unusually large vWF forms in mediating aggregation. Endogenous
released platelet vWF forms, as well as exogenous large or unusually large
vWF multimers, must bind to both glycoproteins Ib and the IIb/IIIa complex
to produce aggregation. Shear- induced aggregation is the result of shear
stress alteration of platelet surfaces, rather than of shear effects on vWF
multimers. It is mediated by either large plasma-type vWF multimers,
endogenous released platelet vWF forms, or unusually large vWF multimers
derived from endothelial cells, requires ADP, and is not inhibited
significantly by aspirin. This type of aggregation may be important in
platelet thrombus formation within narrowed arterial vessels, and may
explain the limited therapeutic utility of aspirin in arterial thrombosis.
Volume 71,
Issue 5,
pp. 1366-1374,
05/01/1988
Copyright © 1988 by The American Society of Hematology
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