Amniotic levels of nitric oxide in women with fetal intrauterine growth restriction.

OBJECTIVE: Many biochemical observations have shown that nitric oxide (NO) is involved in the vascular angiogenic activity of the fetoplacental unit. The aim of this study was to determine whether NO is implicated in the pathogenesis of intrauterine growth restriction (IUGR). METHODS: We retrospectively assessed amniotic fluid NO from second-trimester amniocentesis of 20 healthy normotensive women who subsequently developed IUGR and 20 controls. The same women were re-assessed at the third trimester when IUGR had developed and when the same 20 controls had shown normal pregnancy. Amniotic fluid NO was detected by discontinuous spectrophotometry and the Griess reaction. RESULTS: At the second trimester, NO levels in women with subsequent IUGR were significantly lower than in controls (4.1 +/- 0.2 microg/mg creatinine vs. 6.02 +/- 1.57 microg/mg creatinine, p < 0.001). At the third trimester, in women with IUGR, NO levels were significantly higher than in normal pregnancies (7.4 +/- 1.5 vs. 5.02 +/- 0.9 microg/mg creatinine, p < 0.001), and directly correlated with gestational age when growth restriction was diagnosed (r = 0.69, p < 0.001). CONCLUSIONS: Low levels of NO during the early second trimester may represent an impaired stimulus to vascular formation and endothelial regulation, inducing placental disease and subsequent fetal growth restriction. High levels of amniotic fluid NO during the third trimester may represent a compensation factor for maintaining adequate uteroplacental perfusion in pregnancies with IUGR.

Amniotic levels of vascular endothelial growth factor and nitric oxide at the second trimester in Down's syndrome.

OBJECTIVE: Since placentae in trisomy 21 show trophoblastic hypoplasia and hypovascularity, we investigated amniotic fluid vascular endothelial growth factor (VEGF) and nitric oxide (NO) in normal pregnancy and pregnancy complicated by trisomy 21. Furthermore, we investigated a possible role of NO in neurodegeneration of the brain in Down's syndrome. METHODS: We retrospectively assessed NO and VEGF on mid-trimester amniotic fluid from 15 women who had fetal Down's syndrome, and compared the results with those of 15 controls matched for age and gestation. RESULTS: In pregnancies complicated by trisomy 21, NO levels were significantly higher than in healthy controls (p < 0.001), whereas VEGF levels were significantly lower than in healthy controls (p < 0.05). CONCLUSIONS: Our results suggest that the high levels of NO and the low levels of VEGF observed in the amniotic fluid of fetuses with Down's syndrome may be a sign of an imbalance of placental vascularization and altered endothelial function. Overproduction of NO could contribute to pathological cell death in the central nervous system, a process that has been demonstrated in many neurodegenerative diseases.