PROSTACYCLIN FORMATION IN UMBILICAL ARTERIES IS DOSE-DEPENDENTLY REDUCED BY MATERNAL SMOKING

Abstract

Smoking during pregnancy is associated with increased perinatal morbidity and mortality. Disturbed prostaglandin metabolism might be an important causal factor since the regulation of umbilical-placental blood flow and vasomotor function in the newborn infant is partly prostaglandin-dependent. The aim was to evaluate the impact of maternal smoking on reduced prostacyclin formation in umbilical arteries. Segments from human umbilical arteries were collected at 87 unselected term deliveries. The capacity for prostacyclin formation was estimated, blindly as to smoking habits, using a bioassay technique. In umbilical arteries from infants of non-smoking mothers the prostacyclin-like activity amounted to 81 ± 37 ng/g of umbilical arterial tissue, and in those from all smokers to 66 ± 34 (p<0.05). When smokers were divided into those smoking 10 cigarettes daily or more and those smoking 1-9 cigarettes per day, only umbilical arteries of infants of the heavier smokers showed a significantly lower production of prostacyclin-like activity than the non-smoking group (56 ± 26 ng/g) (p<0.01). Umbilical cord blood levels of nicotine and cotinine were measured and were markedly elevated in the smoking group, but did not correlate to levels of prostacyclin-like activity. A reduced capacity for prostacyclin production in umbilical arteries might imply a reduced capacity for vasodilation and consequently lowered defence against fetal hypoxia.