Effect of preeclampsia on blood pressure in newborn very low birth weight infants.

OBJECTIVE: To test the hypothesis that very low birth infants born to mothers with preeclampsia have higher blood pressure over the first week of life than infants whose mothers did not have preeclampsia. METHOD: Infants born at<1,350 g who survived at least one week were stratified by gestational age ( or= 29 completed weeks) and grouped by the presence or absence of preeclampsia. Highest and lowest systolic and mean and diastolic blood pressures were recorded for each of the first seven days of life. Serial blood pressures were analyzed by repeated measures ANOVA: The presence of hypertension (defined as >or= 3 days with the highest systolic blood pressure>90th percentile for gestational age stratum and day-specific range) was analyzed by binary logistic regression. RESULTS: Infants >or= 29 weeks gestational age born to mothers with preeclampsia had higher blood pressures than did controls. Infants or= 29 weeks gestation. The long-term significance of this finding is not known.

Regulation of FasL/Fas in human trophoblasts: possible implications for chorioamnionitis.

Chorioamnionitis is a common cause of premature birth and is associated with significant morbidity and mortality in the mother and infant. Preterm birth shares similarities with rejection of the fetal allograft, which is characterized by increased apoptosis of placental trophoblasts. We hypothesized that there is increased trophoblast apoptosis in chorioamnionitis and that this increased apoptosis is mediated by the Fas ligand (FasL)/Fas pathway. To test our hypothesis, we examined placental villous tissues from patients with chorioamnionitis and used the TUNEL assay to demonstrate enhanced trophoblast apoptosis in patients with chorioamnionitis. When the same samples were stained for Fas, there was increased trophoblast Fas expression in patients with chorioamnionitis. To define the mechanisms responsible for this increase in trophoblast apoptosis, we cultured villous explants from uncomplicated term placentas with proinflammatory cytokines and demonstrated a marked increase in trophoblast apoptosis. By blocking FasL, we reduced tumor necrosis factor alpha-induced and interferon gamma-induced apoptosis. These data suggest that chorioamnionitis is associated with increased trophoblast apoptosis and enhanced trophoblast Fas expression. As a complement to our in vivo study, we demonstrated that cytokine-induced trophoblast apoptosis is mediated in part by the FasL/Fas pathway, suggesting that cytokines promote sensitivity to Fas-mediated apoptosis. These mechanisms may be important in perpetuating inflammation in the placental microenvironment and may contribute to the pathogenesis of chorioamnionitis.