Document Detail


Effects of smoking on fetoplacental-maternal system during pregnancy.
MedLine Citation:
PMID:  6203408     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fetoplacental function and maternal nutritional condition were assessed in order to clarify the mechanism of retarded fetal growth in pregnant women who smoked. Dehydroepiandrosterone sulfate (DHA-S) loading tests and measurements of cotinine, which is a major metabolite of nicotine, were also made. In heavy smokers, urinary estriol and serum levels of human placental lactogen (hPL) were lower than those in nonsmokers. There was no difference in maternal nutrition between smokers and nonsmokers. Heavy smokers demonstrated a lower conversion of DHA-S to estradiol than did nonsmokers. Levels of cotinine in maternal blood and umbilical cord blood of heavy smokers were remarkably higher than those in nonsmokers. Microscopic examination showed atrophic and hypovascular changes in placental villi from mothers who smoked. These results suggest that retarded fetal growth in heavy smokers is due to impairment of uteroplacental circulation as a result of the vasoconstricting effect of nicotine.
Fetoplacental function and maternal nutritional status were assessed in order to clarify the mechanism of retarded fetal growth in pregnant women who smoked. Dehydroepiandrosterone sulfate (DHA-S) loading tests and measurements of cotinine, a major metabolite of niccotine, were also made. In heavy smokers, urinary estriol and serum levels of human placental lactogen (hPL) were lower than those in nonsmokers. There was no difference in maternal nutrition between smokers and nonsmokers. Heavy smokers demonstrated a lower conversion of DHA-S to estradiol than did nonsmokers. Levels of cotinine in maternal blood and umbilical cord blood of heavy smokers were remakably higher than those in nonsmokers. Microscopic examination showed atrophic and hypovascular changes in placental villi from mothers who smoked. These results suggest that retarded fetal growth in heavy smokers is due to impairment of uteroplacental circulation as a ressult of the vasoconstricting effect of nicotine.
Authors:
M Mochizuki; T Maruo; K Masuko; T Ohtsu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of obstetrics and gynecology     Volume:  149     ISSN:  0002-9378     ISO Abbreviation:  Am. J. Obstet. Gynecol.     Publication Date:  1984 Jun 
Date Detail:
Created Date:  1984-07-13     Completed Date:  1984-07-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370476     Medline TA:  Am J Obstet Gynecol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  413-20     Citation Subset:  AIM; IM; J    
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MeSH Terms
Descriptor/Qualifier:
Birth Weight
Blood Glucose
Chorionic Villi / drug effects,  pathology
Copper / blood
Cotinine / blood,  urine
Dehydroepiandrosterone / metabolism
Estriol / urine
Female
Fetal Blood / analysis
Fetus / drug effects,  physiology*
Growth
Humans
Infant, Newborn
L-Lactate Dehydrogenase / blood
Nicotine / pharmacology*
Placental Lactogen / blood
Pregnancy
Smoking*
Toxemia / metabolism
alpha-Fetoproteins / blood
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/alpha-Fetoproteins; 486-56-6/Cotinine; 50-27-1/Estriol; 53-43-0/Dehydroepiandrosterone; 54-11-5/Nicotine; 7440-50-8/Copper; 9035-54-5/Placental Lactogen; EC 1.1.1.27/L-Lactate Dehydrogenase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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