Both physical and chemical factors can influence the activity of platelets
and coagulation factors responsible for the formation of thrombotic and hem
ostatic masses in the vicinity of an injured vessel wall. Studies performed
in controlled shear devices (viscometers) have indicated that physical fac
tors alone can induce platelet aggregation, even in the absence of exogenou
s chemical factors. The physical considerations which appear to be importan
t for the local activation of hemostatic/thrombotic mechanisms appear to be
related to the magnitude of the shear rate/stress, the duration of the app
lied physical force and the local geometry. Blood flow alone has multiple i
nfluences on platelet and coagulative mechanisms. It has been well establis
hed that at physiologically encountered shear conditions, increases in the
local shear rate enhance the attachment of platelets to the vessel wall and
the growth of platelet aggregates on adherent platelets. In contrast, incr
eases in local shear conditions inhibit the production of fibrin formation
on surfaces where tissue factor (TF) is exposed. At levels of shear rate/st
ress high as compared to normal physiological conditions, but comparable to
those observed at the apex of severely stenosed vessels, platelet aggregat
e formation is dependent on the duration of the exposure time. Considerable
advances in our understanding of flow-related mechanisms have evolved from
the use of well-defined perfusion chambers employing parallel flow streaml
ines. However, processes leading to hemostasis and thrombosis generally occ
ur in more complicated flow situations where flow streamlines are not paral
lel and in which abnormally high, as well as abnormally low, shear rates an
d shear stress levels may be encountered in close proximity to each other.
(C) 1998 Elsevier Science Ltd.