Glucocorticoid treatment does not alter early cardiac adaptations to growth restriction in preterm sheep fetuses
Article first published online: 17 JUN 2012
© 2012 The Authors BJOG An International Journal of Obstetrics and Gynaecology © 2012 RCOG
BJOG: An International Journal of Obstetrics & Gynaecology
Volume 119, Issue 8, pages 906–914, July 2012
How to Cite
Tare, M., Miller, S., Wallace, E., Sutherland, A., Yawno, T., Coleman, H., Jenkin, G. and Parkington, H. (2012), Glucocorticoid treatment does not alter early cardiac adaptations to growth restriction in preterm sheep fetuses. BJOG: An International Journal of Obstetrics & Gynaecology, 119: 906–914. doi: 10.1111/j.1471-0528.2012.03309.x
- Issue published online: 17 JUN 2012
- Article first published online: 17 JUN 2012
- Accepted 15 January 2012.
- fetal growth restriction;
- ischaemia/reperfusion infarct area;
- Langendorff heart
Please cite this paper as: Tare M, Miller S, Wallace E, Sutherland A, Yawno T, Coleman H, Jenkin G, Parkington H. Glucocorticoid treatment does not alter early cardiac adaptations to growth restriction in preterm sheep fetuses. BJOG 2012;119:906–914.
Objective To study the consequences of glucocorticoid treatment in fetal growth restriction (FGR) on cardiac function.
Methods Growth restriction was induced in sheep fetuses using single umbilical artery ligation (SUAL) on days 105–110 of gestation (term 147). Control fetuses were not ligated. Betamethasone (BM) (11.4 mg intramuscularly) or saline was administered to ewes on days 5 and 6 after surgery. Ewes were anaesthetised on day 7, the fetuses were removed, and their hearts were mounted on a Langendorff apparatus. Balloon catheters were inserted into the right and left ventricles.
Outcome measures Ventricular contractile function and infarct area following ischaemia/reperfusion.
Results The SUAL resulted in FGR (body weight 77% of control). The FGR was associated with increases in basal left ventricular pressure development and rates of contraction and relaxation. Right ventricular contraction was unaffected. Following brief ischaemia/reperfusion, the infarct area in FGR hearts was increased four-fold compared with controls. Antenatal BM resulted in a proportional increase in heart size and coronary flow, especially in FGR fetuses, and left ventricular pressure and heart rate responses to β-adrenoceptor activation were increased.
Conclusions Fetal hearts rapidly adapt to FGR to maintain substrate delivery to the brain and heart. The FGR greatly enhanced the area of ischaemia, with implications for susceptibility in postnatal life. Antenatal BM treatment does not interfere with these cardiac changes but appears to increase left ventricle β-adrenoceptor responsiveness, which may render the offspring vulnerable to subsequent cardiac dysfunction.