Sc. Birnbaum et al., NICOTINE-INDUCED OR EPINEPHRINE-INDUCED UTEROPLACENTAL VASOCONSTRICTION AND FETAL GROWTH IN THE RAT, Toxicology, 94(1-3), 1994, pp. 69-80
We examined the relationship between nicotine-induced vasoconstriction
in pregnant rat darns and fetal growth during the third trimester of
pregnancy. Pregnant rats were continuously treated between days 13 and
19 of gestation with either nicotine (9.6, 4.8 or 2.4 mg/kg/day), epi
nephrine (0.72 mu g/kg/day), or saline via continuous infusion from a
subcutaneously implanted osmotic minipump. Placental weights in rats t
reated with high dose nicotine and dams' body weights were severely re
duced. However, fetal weights were not affected. Blood flows in uterus
and placenta were quantified by measurement of tissue content of Sr-8
5-labelled microspheres injected via a carotid artery catheter: Both n
icotine and epinephrine caused a significant reduction(> 40%) in uteri
ne and placental blood flow. We conclude that vasoconstriction alone a
s a result of nicotine or epinephrine administration during the last t
rimester of gestation does not necessarily reduce nutrient supply to t
he fetus and does not affect fetal growth in rats.