Role of von Willebrand factor in mediating platelet-vessel wall interaction
at low shear rate; the importance of perfusion conditions
L Badimon, JJ Badimon, VT Turitto and V Fuster
Division of Cardiology, Mount Sinai School of Medicine, New York, NY.
We have previously observed that von Willebrand factor (vWF) plays an
important role in platelet deposition on subendothelium at low values of
wall shear rate (200 to 400 seconds-1). In the present study, we have
investigated the mechanism responsible for such a defect in platelet
deposition at low shear rates in the absence of vWF. Blood from both normal
and von Willebrand's disease (vWD) animals was exposed to
de-endothelialized aorta from normal pigs for a range of shear rates (200
to 3,000 seconds-1) and exposure times (three to 30 minutes) in a tubular
perfusion chamber. Variations in the method of inhibiting coagulation
(none, heparin, citrate, hirudin, and EDTA) and of perfusing blood (in
vitro v ex vivo) were compared by determining the influence of wall shear
rate and vWF on the deposition of 111In-labeled platelets on
subendothelium. Whereas platelet deposition was reduced in the absence of
vWF for all experimental variations at high shear rates (greater than 850
seconds-1), a defect was observed at low shear rates only when heparinized
blood was exposed by means of an ex vivo perfusion system. Maximum
sensitivity of the measurement occurs under ex vivo perfusion conditions
due to the reduced ability of platelets to deposit in normal blood when
recirculated in vitro. Our results indicate that vWF mediates
platelet-vessel wall interaction even at low shear rates and that such
effect can only be observed in systems where platelet function is minimally
affected by the experimental conditions.
Volume 73,
Issue 4,
pp. 961-967,
03/01/1989
Copyright © 1989 by The American Society of Hematology
