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Disseminated intravascular coagulation in rabbits induced by administration
of endotoxin or tissue factor: effect of anti-tissue factor antibodies and
measurement of plasma extrinsic pathway inhibitor activity
TA Warr, LV Rao and SI Rapaport
Department of Medicine, University of California, San Diego.
Rabbits were given polyclonal anti-tissue factor (TF) immunoglobulin G
(IgG) before an injection of endotoxin to test the hypothesis that TF
triggers disseminated intravascular coagulation (DIC) after endotoxin. The
rabbits had been prepared with cortisone to develop DIC after one injection
of endotoxin. Anti-TF IgG substantially reduced the falls in fibrinogen,
factors V and VIII, and platelets noted in control rabbits given preimmune
IgG before endotoxin. At autopsy 24 hours later, fibrin was present in
glomerular capillaries of 4 of 5 control rabbits, but in none of 11 rabbits
given anti-TF IgG. DIC was also induced in a second group of rabbits by the
infusion, over 4 hours, of 1 microgram/kg of purified, reconstituted rabbit
brain TF. This resulted in striking falls in plasma fibrinogen, factors V,
and VIII that were diminished, but not prevented by prior treatment with
anti-TF IgG. Circulating activated factor VII, induced by either TF
infusion or endotoxin, could not be detected after DIC. Mean plasma
extrinsic pathway inhibitor (EPI) activity did not fall significantly after
endotoxin, and only to about 65% of the preinfusion after infusion of TF.
Thus, DIC induced by both agents proceeded despite nearly normal plasma EPI
levels. Because EPI neutralizes factor VIIa/TF in vitro only after a short
lag period, the DIC that persisted for up to 6 hours after injection of
endotoxin suggests that TF activity continued to be generated during this
period on cells to which the circulating blood was exposed. All animals
given endotoxin became ill with cyanosis, tachypnea, cold ears, and
diarrhea, regardless of whether they had received anti-TF IgG to attenuate
DIC. Infusion of TF caused some animals to die acutely with pulmonary
arterial thromboses, but surviving animals did not appear ill. The findings
support the hypothesis that exposure of blood to TF triggers DIC after
endotoxin, but is not important for the pathogenesis of endotoxin-induced
shock.
Volume 75,
Issue 7,
pp. 1481-1489,
04/01/1990
Copyright © 1990 by The American Society of Hematology
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