title: Maternal and fetal platelet activation in normal pregnancy.
abstract: OBJECTIVE
  To study the platelet activation phase in normal pregnant women and their fetuses, both in vivo under basal conditions and in vitro after stimulation by adenosine diphosphate (ADP), a weak agonist, and U46619, a strong one.
  
  
  METHODS
  Platelet function was investigated in 39 normal pregnant women and their fetuses undergoing fetal blood sampling at 18-37 weeks' gestation, using flow cytometry and the anti-GMP140 monoclonal antibody. This combined technique allows platelets to be investigated in small aliquots of whole blood, and it detects platelet secretion regardless of aggregation. In all cases, the percentage of activated platelets was determined under basal conditions and after addition of platelet agonists: ADP at concentrations of 10 and 50 mumol/L, and U46619, a stable analogue of thromboxane A2, at 1 mumol/L.
  
  
  RESULTS
  Compared to nonpregnant controls, pregnant women had a significantly lower percentage of activated platelets after addition of U46619 (P = .02). Compared to their mothers, fetuses had significantly inferior platelet activation after addition of both platelet-activating factors at all concentrations used (ADP 10 mumol/L, P < .0001 and ADP 50 mumol/L, P < .0001; U46619, P < .0001). Maternal and fetal platelet activation did not change with duration of gestation. In the fetus, the percentage of activated platelets did not correlate with hematocrit, pH, or oxygen pressure, but it correlated significantly with platelet count after addition of U46619 (r = 0.45, P = .006).
  
  
  CONCLUSIONS
  Decreased platelet activation in both pregnant women and fetuses suggests the action of a plasma factor that selectively inhibits prostaglandin-dependent activation. Prostacyclin, which is known to decrease platelet aggregation and release reactions caused by agonists, might have a greater inhibitory effect in the fetus than in the mother, or be present in larger amounts in the fetus.
authors.affiliation: 1st Department of Obstetrics and Gynecology, University of Milano, Italy.
authors.forename: U
authors.initials: U
authors.lastname: Nicolini
authors.forename: D
authors.initials: D
authors.lastname: Guarneri
authors.forename: G A
authors.initials: GA
authors.lastname: Gianotti
authors.forename: C
authors.initials: C
authors.lastname: Campagnoli
authors.forename: P G
authors.initials: PG
authors.lastname: Crosignani
authors.forename: L
authors.initials: L
authors.lastname: Gatti
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D005260:Female; D005312:Fetal Blood; D005333:Fetus / Q000502:physiology*; D006801:Humans; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy / Q000097:blood / Q000502:physiology*; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D012044:Regression Analysis; D013928:Thromboxane A2 / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D011450:Prostaglandin Endoperoxides, Synthetic; D013928:Thromboxane A2; D000244:Adenosine Diphosphate; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid