Abstract
BackgroundFetal Growth Restriction is often associated with a feto-placental vascular dysfunction conceivably involving endothelial cells. Our study aimed to verify this pathogenic role for feto-placental endothelial cells and, coincidentally, demonstrate any abnormality in the nitric oxide system.MethodsPrenatal assessment of feto-placental vascular function was combined with measurement of nitric oxide (in the form of S-nitrosohemoglobin) and its nitrite byproduct, and of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine. Umbilical vein endothelial cells were also harvested to determine their gene profile. The study comprised term pregnancies with normal (n = 40) or small-for-gestational-age (n = 20) newborns, small-for-gestational-age preterm pregnancies (n = 15), and bi-chorial, bi-amniotic twin pregnancies with discordant fetal growth (n = 12).ResultsUmbilical blood nitrite (p<0.001) and S-nitrosohemoglobin (p = 0.02) rose with fetal growth restriction while asymmetric dimethylarginine decreased (p = 0.003). Nitrite rise coincided with an abnormal Doppler profile from umbilical arteries. Fetal growth restriction umbilical vein endothelial cells produced more nitrite and also exhibited reciprocal changes in vasodilator (upwards) and vasoconstrictor (downwards) transcripts. Elevation in blood nitrite and S-nitrosohemoglobin persisted postnatally in the fetal growth restriction offspring.ConclusionFetal growth restriction is typified by increased nitric oxide production during pregnancy and after birth. This response is viewed as an adaptative event to sustain placental blood flow. However, its occurrence may modify the endothelial phenotype and may ultimately represent an element of risk for cardiovascular disease in adult life.
Highlights
[6] Among the several agents controlling this vascular district, nitric oxide (NO) appears most important for its known role under normal conditions and as a target for pathological insults, [7] including possibly events that are identified with the development of Fetal growth restriction (FGR).8,9
NO2 elevation was marked with body weight (BW) below the 10th centile (Fig. 1A)
NOHb was elevated in umbilical blood of FGR pregnancies, regardless of whether it originated from the artery or the vein (Figg. 1C and 1D)
Summary
Fetal growth restriction (FGR) complicates up to 8% of pregnancies and carries high perinatal morbidity and mortality. [1] Infants born as small-for-gestational-age (SGA) present a greater risk for cardiovascular disease during adulthood. [2] No definite explanation is available for the latter occurrence, a deranged prenatal or perinatal programming of certain mechanisms [3,4,5] may be involved.An alteration of the feto-placental circulation, reportedly involving the endothelium, plays a key part in the onset and progression of FGR. [6] Among the several agents controlling this vascular district, nitric oxide (NO) appears most important for its known role under normal conditions and as a target for pathological insults, [7] including possibly events that are identified with the development of FGR. besides being impaired by a variety of stimuli, NO may have a compensatory function, and several situations in the adult document this possibility. [8].Our objective was to study NO function in pregnancies complicated by FGR. Fetal growth restriction (FGR) complicates up to 8% of pregnancies and carries high perinatal morbidity and mortality. An alteration of the feto-placental circulation, reportedly involving the endothelium, plays a key part in the onset and progression of FGR. [6] Among the several agents controlling this vascular district, nitric oxide (NO) appears most important for its known role under normal conditions and as a target for pathological insults, [7] including possibly events that are identified with the development of FGR.. Our objective was to study NO function in pregnancies complicated by FGR. Fetal Growth Restriction is often associated with a feto-placental vascular dysfunction conceivably involving endothelial cells. Our study aimed to verify this pathogenic role for feto-placental endothelial cells and, coincidentally, demonstrate any abnormality in the nitric oxide system
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
