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The stable prostacyclin analog, iloprost, and prostaglandin E1 inhibit
monocyte procoagulant activity in vitro
DJ Crutchley and MJ Hirsh
Research Division, Miami Heart Institute, FL 33140.
Exposure of human peripheral blood to 100 ng/mL of bacterial endotoxin for
2 hours resulted in a 20-fold increase in monocyte procoagulant activity.
The activity was functionally identified as tissue factor, because it was
not expressed in plasma deficient in factor VII and was specifically
inhibited by a monoclonal antibody directed against human tissue factor.
When the stable prostacyclin analog, iloprost, was added to blood 30
minutes before endotoxin, a dose-dependent inhibition of monocyte
procoagulant activity occurred, with an I50 of 20 nmol/L. Prostaglandin E1
(PGE1) produced similar effects, with an I50 of 150 nmol/L. Exposure of
THP-1 monocytic cells to 100 ng/mL endotoxin resulted in a threefold
increase in procoagulant activity after 2 hours and a 20-fold increase
after 6 hours. A 30-minute pretreatment with iloprost or PGE1 again
inhibited development of procoagulant activity, with I50 values of 5 nmol/L
and 150 nmol/L, respectively. Treatment of THP-1 cells with iloprost 2
hours after exposure to endotoxin significantly inhibited further increases
in procoagulant activity. Iloprost was less potent under these conditions,
30% inhibition being obtained at 100 nmol/L and 70% at 1 mumol/L. These
results suggest that prostacyclin may be a physiologic modulator of
monocyte tissue factor expression; in addition, its stable analog,
iloprost, may have clinical potential for the treatment of thrombotic
disorders in which elevated monocyte procoagulant activity plays a role.
Volume 78,
Issue 2,
pp. 382-386,
07/15/1991
Copyright © 1991 by The American Society of Hematology
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