| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
The Pediatric Heart Lung Center, Departments of 1 Pediatrics and 2 Internal Medicine, University of Colorado School of Medicine, Denver, Colorado 80262; and 3 Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Prolonged infusions of 17
-estradiol
reduce fetal pulmonary vascular resistance (PVR), but the effects of
endogenous estrogens in the fetal pulmonary circulation are unknown. To
test the hypothesis that endogenous estrogen promotes pulmonary
vasodilation at birth, we studied the hemodynamic effects of prolonged
estrogen-receptor blockade during late gestation and at birth in fetal
lambs. We treated chronically prepared fetal lambs with ICI-182,780
(ICI, a specific estrogen-receptor blocker, n = 5) or
1% DMSO (CTRL, n = 5) for 7 days and then measured
pulmonary hemodynamic responses to ventilation with low- and
high-fraction inspired oxygen (FIO2). Treatment with ICI did not change basal fetal PVR or arterial blood gas
tensions. However, treatment with ICI abolished the vasodilator
response to ventilation with low FIO2
[change in PVR 
30 ± 6% (CTRL) vs. +10 ± 13%, (ICI),
P < 0.05] without reducing the vasodilator response
to ventilation with high FIO2 [change in
PVR, 73 ± 3% (CTRL) vs. 77 ± 4%, (ICI);
P = not significant]. ICI treatment reduced
prostacyclin synthase (PGIS) expression by 33% (P < 0.05) without altering expression of endothelial nitric oxide synthase
or cyclooxygenase-1 and -2. In situ hybridization and
immunohistochemistry revealed that PGIS is predominantly expressed in
the airway epithelium of late gestation fetal lambs. We conclude that
prolonged estrogen-receptor blockade inhibits the pulmonary vasodilator
response at birth and that this effect may be mediated by
downregulation of PGIS. We speculate that estrogen exposure during late
gestation prepares the pulmonary circulation for postnatal adaptation.
prostacyclin; prostacyclin synthase; cyclooxygenase; newborn
This article has been cited by other articles:
|
|
 |
|
  A. A. Miller, A. A. Hislop, P. J. Vallance, and S. G. Haworth Deletion of the eNOS gene has a greater impact on the pulmonary circulation of male than female mice Am J Physiol Lung Cell Mol Physiol, August 1, 2005; 289(2): L299 - L366. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Korita, H. Itoh, N. Sagawa, S. Yura, M. Yoshida, K. Kakui, M. Takemura, and S. Fujii 17{beta}-Estradiol Up-Regulates Prostacyclin Production in Cultured Human Uterine Myometrial Cells Via Augmentation of Both Cyclooxygenase-1 and Prostacyclin Synthase Expression Reproductive Sciences, October 1, 2004; 11(7): 457 - 464. [Abstract] [PDF]
|
|
|
|
|
|
V. Hampl, J. Bibova, I. Ostadalova, V. Povysilova, and J. Herget Gender differences in the long-term effects of perinatal hypoxia on pulmonary circulation in rats Am J Physiol Lung Cell Mol Physiol, August 1, 2003; 285(2): L386 - L392. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. G. Konduri and J. Mattei Role of oxidative phosphorylation and ATP release in mediating birth-related pulmonary vasodilation in fetal lambs Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1600 - H1608. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
