|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Neurology
2 Institute of Laboratory Animal Science, Friedrich Schiller University, Jena, Germany
3Center for Pregnancy and Newborn Research, Department of Obstetrics and Gynecology, University of Texas Health Sciences Center, San Antonio, TX, USA
Synthetic glucocorticoids are administered to pregnant women in premature labour to accelerate fetal lung maturation at a time when fetal cerebrovascular and endocrine systems are maturing. Exposure to glucocorticoids at 0.80.9 of gestation increases peripheral and cerebrovascular resistance (CVR) in fetal sheep. We examined whether the increase of CVR and its adverse effect on cerebral blood flow (CBF) depend on the current level of maturation of the pituitaryadrenal axis and the cerebrovascular system. Using fluorescent microspheres, regional CBF was measured in 11 brain regions before and 24 h and 48 h after the start of 3.3 µg kg1 h1 betamethasone (n = 8) or vehicle (n = 7) infusions to fetal sheep at 0.73 of gestation. Hypercapnic challenges were performed before and 24 h after the onset of betamethasone exposure to examine betamethasone effects on cerebrovascular reactivity. Betamethasone exposure decreased CBF by approximately 40% in all brain regions after 24 h of infusion (P < 0.05). The decline in CBF was mediated by a CVR increase of 111 ± 16% in the cerebral cortex and 129 ± 29% in subcortical regions (P < 0.05). Hypercapnic cerebral vasodilatation and associated increase in CBF were blunted (P < 0.05). Fetal CBF recovered after 48 h of betamethasone administration. There were no differences in glucocorticoid induced CBF and CVR changes compared with our previous findings at 0.87 of gestation. We conclude that the cerebrovascular effects of antenatal glucocorticoids are independent of cerebrovascular maturation and preparturient increase in activity of the fetal pituitaryadrenal axis.
(Received 18 October 2004;
accepted after revision 11 February 2005;
first published online 17 February 2005)
Corresponding author M. Schwab: Department of Neurology, Friedrich Schiller University, 07740 Jena, Germany. Email: matthias.schwab{at}med.uni-jena.de
This article has been cited by other articles:
![]() |
J. K. Jellyman, D. S. Gardner, C. M. B. Edwards, A. L. Fowden, and D. A. Giussani Fetal cardiovascular, metabolic and endocrine responses to acute hypoxaemia during and following maternal treatment with dexamethasone in sheep J. Physiol., September 1, 2005; 567(2): 673 - 688. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |