Physiological concentrations of nicotine do not affect prostacyclin, thromboxane or PGE production from perfused human umbilical veins

Smoking during pregnancy is associated with a number of maternal and fetal complications. The mechanisms underlying the effects of nicotine on fetal g rowth and develop ment are not known, but may involve decreases in umbilica l-placental blood flow. Prostaglandins are vasoactive mediators that regula te umbilical-placental blood flow and there is evidence that nicotine may a lter prostaglandin production. Thus, alterations in vasoactive prostaglandi ns from the human umbilical vein may explain nicotine-induced decreases in vessel blood flow and may under lie some of the negative effects of nicotin e on the fetus. This study was designed to deter mine the relationship betw een nicotine and human umbilical vein prostaglandin production. Prostacycli n, thromboxane and prostaglandin E were measured from human umbilical veins collected from women at the time of cesarean section. Vessels were perfuse d with either vehicle (Dulbecco's modified Eagle's media), 5 mM, 10 mM or 2 0 mM nicotine for 60 minutes. Samples were collected from the perfusate aft er 5, 15, 30 and 60 minutes of perfusion, and prostaglandins were measured by radioimmunoassay. Data were analyzed by ANOVA. Perfusion with 10 mM or 2 0 mm significantly reduced prostacyclin product ion by the human umbilical veins, but nicotine did not affect prostaglandin E. The effects of nicotine on thromboxane were less clear. However, nicotine concentrations required to illicit an effect on prostacyclin production were much larger than circu lating levels associated with smoking, so it is only pharmacological concen trations that have a significant effect. Thus, nicotine-induced alterations in umbilical vein prostaglandin production does not appear to be a mechani sm by which nicotine adversely affects fetal growth and development.