NITRIC-OXIDE SYNTHASE ACTIVITIES IN PLACENTAL TISSUE FROM NORMOTENSIVE, PREECLAMPTIC AND GROWTH-RETARDED PREGNANCIES

Citation
Nh. Morris et al., NITRIC-OXIDE SYNTHASE ACTIVITIES IN PLACENTAL TISSUE FROM NORMOTENSIVE, PREECLAMPTIC AND GROWTH-RETARDED PREGNANCIES, British journal of obstetrics and gynaecology, 102(9), 1995, pp. 711-714
Citations number
28
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
03065456
Volume
102
Issue
9
Year of publication
1995
Pages
711 - 714
Database
ISI
SICI code
0306-5456(1995)102:9<711:NSAIPT>2.0.ZU;2-1
Abstract
Objective To measure nitric oxide synthase activity in tissues from th e placenta, placental bed and umbilical cord at delivery in normal and complicated pregnancies. Design A prospective blinded study. Setting The obstetric departments of three London teaching hospitals. Subjects Samples of whole placenta, dissected stem villous arteries, umbilical cord vessels and the placental bed of the uterus were collected at de livery and assayed for nitric oxide synthase activity. Samples of plac enta were taken from ten normotensive, six pre-eclamptic and eight gro wth retarded pregnancies, and stem villous arteries from a further sev en normotensive pregnancies. Results There was minimal placental bed n itric oxide synthase activity in each group. Placental villous homogen ates from pregnancies complicated by pre-eclampsia and fetal growth re tardation had significantly lower activities of nitric oxide synthase than those from normotensive women with appropriately grown babies. Th ere were no significant differences in calcium dependent or calcium in dependent nitric oxide synthase activities in the umbilical vein and a rtery in the normal or in the pre-eclamptic groups. However, there was significantly more calcium dependent than calcium independent nitric oxide synthase in the umbilical veins in all groups. Conclusions Local nitric oxide production in the placental bed of the uterus is unlikel y to contribute substantially to the low resting vascular tone in the uteroplacental circulation However, a relative deficiency of placental nitric oxide in pregnancies complicated by fetal growth retardation a nd pre-eclampsia may contribute to the development of the high impedan ce fetoplacental circulation found in these conditions.