NICOTINE-INDUCED OR EPINEPHRINE-INDUCED UTEROPLACENTAL VASOCONSTRICTION AND FETAL GROWTH IN THE RAT

Citation
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
Citations number
24
Categorie Soggetti
Toxicology,"Pharmacology & Pharmacy
Journal title
ISSN journal
0300483X
Volume
94
Issue
1-3
Year of publication
1994
Pages
69 - 80
Database
ISI
SICI code
0300-483X(1994)94:1-3<69:NOEUV>2.0.ZU;2-R
Abstract
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.