title: Effects of smoking on fetoplacental-maternal system during pregnancy.
abstract: 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.
mesh_terms: D001724:Birth Weight; D001786:Blood Glucose; D002824:Chorionic Villi / Q000187:drug effects / Q000473:pathology; D003300:Copper / Q000097:blood; D003367:Cotinine / Q000097:blood / Q000652:urine; D003687:Dehydroepiandrosterone / Q000378:metabolism; D004964:Estriol / Q000652:urine; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005333:Fetus / Q000187:drug effects / Q000502:physiology*; D006128:Growth; D006801:Humans; D007231:Infant, Newborn; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009538:Nicotine / Q000494:pharmacology*; D010928:Placental Lactogen / Q000097:blood; D011247:Pregnancy; D012907:Smoking; D014115:Toxemia / Q000378:metabolism; D000509:alpha-Fetoproteins / Q000097:blood
chemical_list: D001786:Blood Glucose; D000509:alpha-Fetoproteins; D003687:Dehydroepiandrosterone; D009538:Nicotine; D003300:Copper; D010928:Placental Lactogen; D007770:L-Lactate Dehydrogenase; D004964:Estriol; D003367:Cotinine