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Initiation of the tissue factor pathway of coagulation in the presence of
heparin: control by antithrombin III and tissue factor pathway inhibitor
J Jesty, A Lorenz, J Rodriguez and TC Wun
Department of Medicine, State University of New York, Stony Brook, NY.
Activation of factor X by both the unactivated tissue factor:factor VII
complex (TF:VII) and the activated tissue factor:factor VIIa complex
(TF:VIIa) has been studied in the presence of tissue factor pathway
inhibitor (TFPI), antithrombin III (ATIII), and heparin. At near-plasma
concentrations of TFPI, ATIII, and factor X, factor X activation that
occurs in response to TF:VII is essentially abolished in the presence of
heparin (0.5 micromol/L). This effect requires both inhibitors, acting on
different targets: (1) ATIII, which in the presence of heparin blocks the
activation of TF:VII, and (2) TFPI, which inhibits the TF:VIIa that is
generated. In the absence of ATIII, TFPI alone with heparin reduces but
does not abolish factor X activation. Conversely, in the absence of TFPI,
ATIII + heparin reduces but does not abolish TF:VIIa generation and allows
continuing activation of factor X. These results indicated that when the
unactivated TF:VII complex is the initiating stimulus, heparin-dependent
reduction in the rate and extent of factor X activation requires both ATIII
and TFPI. In contrast, if TF:VIIa is used to initiate activation, only TFPI
is involved in its regulation.
Volume 87,
Issue 6,
pp. 2301-2307,
03/15/1996
Copyright © 1996 by The American Society of Hematology
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