Objective: To measure platelet activation in normal pregnancy, before
and after stimulation with agonists, with a whole blood flow cytometri
c technique. Methods: In a cross-sectional study, 5 mt of whole blood
was collected from healthy volunteers (nine in the first trimester, te
n in the second trimester, 35 in the third trimester, and 32 nonpregna
nt controls). Platelets were treated with an agonist (thrombin or U-46
619, a thromboxane A2 analogue) or buffer and were exposed to saturati
ng concentrations of monoclonal antibodies directed against platelet m
embrane glycoproteins (GPs): 7E3 (fibrinogen receptor GPIIb/IIIa), S12
(alpha granule marker P-selectin), and 6D1 (van Willebrand factor rec
eptor GPIb). Mean fluorescence intensity was determined for 5000 plate
lets per sample by using a flow cytometer. Results: In the absence of
agonist, no significant difference between groups was found in antibod
y binding. At no stage of pregnancy were circulating activated platele
ts detected. platelets from third-trimester subjects bound significant
ly less 7E3 than platelets of controls or of first-or second-trimester
subjects after stimulation with high-dose thrombin (P < .05 for all c
omparisons). Down-regulation of 6D1 on platelets after stimulation wit
h high-dose U-46619 was significantly greater in third-trimester gravi
das than in controls or first-trimester subjects (P < .05). Conclusion
: Pregnancy does not increase the percentage of activated platelets in
the circulation. Platelet reactivity is altered in the third trimeste
r, as evidenced by decreased antibody binding to a fibrinogen receptor
epitope and enhanced down-regulation of a von Willebrand factor recep
tor epitope. (C) 1997 by The American College of Obstetricians and Gyn
ecologists.