Objective: In preeclampsia markers of endothelial activation (e.g., increased cellular fibronectin and activities that alter in vitro endothelial function (e.g., stimulation of nitric oxide and prostacyclin generation) are increased in the maternal circulation. We tested preeclamptic infant blood for these markers and activities and correlated these findings with fetal growth.
Study design: Plasma was obtained from 17 term nulliparcus preeclamptic and normal pregnant women and their infants and from 8 additional preeclamptic mother-baby pairs from earlier gestations. Plasma cellular fibronectin and production of nitric oxide and prostacyclin by cultured endothelial cells exposed to 2% plasma were measured.
Results: Cellular fibronectin was higher in maternal plasma of preeclamptic than nonpregnant women (6.1 +/- 0.29 vs 4.2 +/- 0.27 microgram/ml, p < 0.01), as were stimulated endothelial nitric oxide and prostacyclin production (nitric oxide 42.5 +/- 3.9 vs 26.9 +/- 2.3 nmol nitrite/microgram protein/24 hours, p < 0.05; prostacyclin 261.7 +/- 31.2 vs 151.9 +/- 18.7 pg prostaglandin F1 alpha/microgram protein/24 hours, p < 0.05). In the preeclamptic infants cellular fibronectin was also greater (3.3 +/- 0.15 vs 2.6 +/- 0.14 microgram/ml, p < 0.01), as was endothelial nitric oxide production in response to the plasma (24.4 +/- 1.1 vs 21.4 +/- 0.09 mumol/L nmol nitrite/microgram protein/24 hours, p < 0.05). Prostacyclin production was not significantly different. In preeclamptic infants across a wide gestational age there was no correlation of endothelial activation and fetal growth.
Conclusions: Infants of women with preeclampsia may be affected by endothelial dysfunction, as well as reduced uteroplacental perfusion.