Document Detail


Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction.
MedLine Citation:
PMID:  23028913     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: 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.
METHODS: Prenatal 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).
RESULTS: Umbilical 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.
CONCLUSION: Fetal 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.
Authors:
Silvia Pisaneschi; Francesca A L Strigini; Angel M Sanchez; Silvia Begliuomini; Elena Casarosa; Andrea Ripoli; Paolo Ghirri; Antonio Boldrini; Bruno Fink; Andrea R Genazzani; Flavio Coceani; Tommaso Simoncini
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-09-27
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-02-28     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e45294     Citation Subset:  IM    
Affiliation:
Division of Obstetrics and Gynecology, Department of Reproductive Medicine and Child Development, University of Pisa, Pisa, Italy.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Adult
Arginine / analogs & derivatives*,  blood
Endothelial Cells / metabolism
Endothelium, Vascular / metabolism,  ultrasonography
Female
Fetal Blood / metabolism*
Fetal Growth Retardation / blood*,  genetics,  ultrasonography
Fetus
Gene Expression Profiling
Hemoglobins / metabolism
Humans
Infant, Low Birth Weight
Infant, Newborn
Nitric Oxide / biosynthesis*
Nitric Oxide Synthase Type III / genetics,  metabolism*
Nitrites / blood
Placenta / metabolism*
Pregnancy
Reverse Transcriptase Polymerase Chain Reaction
Umbilical Arteries / metabolism,  ultrasonography
Umbilical Veins / metabolism,  ultrasonography
Up-Regulation
Chemical
Reg. No./Substance:
0/Hemoglobins; 0/Nitrites; 0/S-nitrosohemoglobin; 10102-43-9/Nitric Oxide; 30315-93-6/N,N-dimethylarginine; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase Type III
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