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Evidence for tissue factor-dependent activation of the classic extrinsic
coagulation mechanism in blood obtained from bleeding time wounds
HJ Weiss and B Lages
Department of Medicine, St Luke's-Roosevelt Hospital Center, New York, NY
10019.
The activation of platelets and the coagulation mechanism was studied by
collecting blood from a standard bleeding time incision at 30-second
intervals and measuring the plasma concentrations of fibrinopeptide A
(FPA), platelet factor 4 (PF4), and thromboxane B2 (TxB2). FPA was observed
in the first samples (30 to 60 seconds) obtained, increased progressively
until cessation of bleeding, and was markedly diminished after heparin
administration, thus indicating that thrombin formation occurs early in
incisional blood. PF4 increased monotonically throughout blood sampling,
whereas the major increase in TxB2 appeared near the cessation of bleeding.
The initial increase in FPA content occurred normally in patients with
deficiencies of either factor IX or VIII, was markedly diminished in
patients with factor X or V deficiency, and was delayed in patients with
factor VII deficiency. These studies suggest that tissue factor activation
of the classic (activation of factor X) extrinsic coagulation mechanism
occurs as an early event during the arrest of bleeding from bleeding time
incisions. The relation of the aforementioned to platelet activation is
less clear because there was no consistent correlation between decreased
FPA formation and impaired PF4 secretion or TxB2 production. In fact, the
latter were normal in some subjects with the most impaired FPA formation,
which suggests that both collagen and thrombin, perhaps synergistically,
may contribute to platelet activation during the primary arrest of
bleeding.
Volume 71,
Issue 3,
pp. 629-635,
03/01/1988
Copyright © 1988 by The American Society of Hematology

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