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Glucocorticoid treatment does not alter early cardiac adaptations to growth restriction in preterm sheep fetuses
Author(s) -
Tare M,
Miller SL,
Wallace EM,
Sutherland AE,
Yawno T,
Coleman HA,
Jenkin G,
Parkington HC
Publication year - 2012
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2012.03309.x
Subject(s) - medicine , fetus , glucocorticoid , cardiology , ischemia , ligation , endocrinology , cardiac function curve , pregnancy , biology , heart failure , genetics
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. Setting Laboratory. Sample Sheep. 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.