EVIDENCE OF ENDOTHELIAL ACTIVATION AND ENDOTHELIAL ACTIVATORS IN CORD-BLOOD OF INFANTS OF PREECLAMPTIC WOMEN

OBJECTIVE: In preeclampsia markers of endothelial activation (e.g., in creased cellular fibronectin and activities that alter in vitro endoth elial function (e.g., stimulation of nitric oxide and prostacyclin gen eration) are increased in the maternal circulation. We tested preeclam ptic infant blood for these markers and activities and correlated thes e findings with fetal growth. STUDY DESIGN: Plasma was obtained from 1 7 term nulliparous preeclamptic and normal pregnant women and their in fants and from 8 additional preeclamptic mother-baby pairs from earlie r gestations. Plasma cellular fibronectin and production of nitric oxi de and prostacyclin by cultured endothelial cells exposed to 2% plasma were measured. RESULTS: Cellular fibronectin was higher in maternal p lasma of preeclamptic than nonpregnant women (6.1 +/- 0.29 vs 4.2 +/- 0.27 mu g/ml, p < 0.01), as were stimulated endothelial nitric oxide a nd prostacyclin production (nitric oxide 42.5 +/- 3.9 vs 26.9 +/- 2.3 nmol nitrite/mu g protein/24 hours, p < 0.05; prostacyclin 261.7 +/- 3 1.2 vs 151.9 +/- 18.7 pg prostaglandin F-1 alpha/mu g protein/24 hours , p < 0.05). In the preeclamptic infants cellular fibronectin was also greater (3.3 +/- 0.15 vs 2.6 +/- 0.14 mu g/ml, p < 0.01), as was endo thelial nitric oxide production in response to the plasma (24.4 +/- 1. 1 vs 21.4 +/- 0.09 mu mol/L nmol nitrite/mu g protein/24 hours, p < 0. 05). Prostacyclin production was not significantly different. In preec lamptic infants across a wide gestational age there was no correlation of endothelial activation and fetal growth. CONCLUSIONS: Infants of w omen with preeclampsia may be affected by endothelial dysfunction, as well as reduced uteroplacental perfusion.