MECHANISM OF FETAL GROWTH-RETARDATION CAUSED BY SMOKING DURING PREGNANCY

  • 1 January 1985
    • journal article
    • research article
    • Vol. 65  (3) , 295-304
Abstract
To clarify the mechanism of retarded fetal growth in smoking pregnant women, feto-placental function and maternal nutritional condition were assessed. Dehydroepiandrosterone sulfate (DHAS) loading test, measurement of cotinine which is a major metabolite of nicotine and pathohistological examination of placental villi were also made to know the effect of smoking on utero-placental circulation. In heavy smokers, urinary estriol and serum hPL [human placental lactogen] levels were lower than those in non-smokers while the maternal nutritional condition was not different from that in non-smokers. In the DHAS loading test, heavy smokers showed lower conversion of DHAS to estradiol. In the non-stress test (NST), bradycardia and/or loss of variability of baseline fetal heart rate were noted after smoking. Levels of cotinine in maternal blood and umbilical cord blood in heavy smokers were markedly higher than those in non-smokers. Microscopic examination showed atrophic and hypovascular changes of placental villi obtained from smoking mothers. Evidently, the retarded fetal growth in heavy smokers is due to the impairment of utero-placental circulation as a result of the vasoconstricting effect of nicotine.

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