| Autor: |
Supramaniam, V. G., Jenkin, G., Loose, J., Wallace, E. M., Miller, S. L. |
| Předmět: |
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| Zdroj: |
BJOG: An International Journal of Obstetrics & Gynaecology; Jan2006, Vol. 113 Issue 1, p102-109, 8p, 3 Charts, 1 Graph |
| Abstrakt: |
Objective To determine whether activin A concentrations are altered in chronic fetal hypoxemia and intrauterine fetal growth restriction (IUGR). Design In vivo animal experimental model. Setting Department of Physiology, Monash University. Population Chronically catherised fetal sheep in late pregnancy. Methods Chronic fetal hypoxia and IUGR were experimentally induced by single umbilical artery ligation (SUAL) in catheterised fetal sheep. Maternal and fetal blood samples and amniotic fluid (AF) samples were collected during surgery and thereafter on alternate days, until the time of delivery for analyte measurement. Fetal blood gas parameters were measured daily. Main outcome measures Plasma and AF was used to analyse activin A, prostaglandin E2 (PGE2) and cortisol and fetal blood gas analysis was undertaken in whole blood. Results SUAL produced asymmetric IUGR and non-acidaemic chronic fetal hypoxia and resulted in preterm labour (129 [3] days). AF activin A concentrations were 10-fold higher in the SUAL group than in controls whereas levels in the fetal and maternal circulations were similar between groups. Conclusions SUAL-induced IUGR and fetal hypoxaemia increases AF activin A. This may be an important adaptive or protective response to IUGR. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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