Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB068

Poster Communications

Fetal hemodynamic response to acute maternal hyperoxygenation in the setting of intrauterine growth restriction

B. S. Saini1, J. R. Darby2, S. R. Perumal3, J. Soo2, M. C. Lock2, C. K. Macgowan4, M. Seed1, J. L. Morrison2

1. Heart Centre, The Hospital for Sick Children, Toronto, Ontario, Canada. 2. Early Origins of Adult Health Research Group, University of South Australia, Adelaide, South Australia, Australia. 3. South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia. 4. Translational Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada.

Introduction: Placental insufficiency results in chronic fetal hypoxemia that leads to intrauterine growth restriction (IUGR) because oxygen delivery to the fetus is an independent determinant of fetal growth (1). Furthermore, IUGR offspring are at an increased risk of adverse perinatal and long-term outcomes, including neurodevelopmental and cardiovascular complications (2). One approach to preventing these negative effects may be to increase fetal oxygenation via maternal hyperoxygenation (MH), which improves outcomes in severely IUGR pregnancies (3). We present the hemodynamic response to acute MH in normoxemic and chronically hypoxemic IUGR fetuses. Methods: At 109-111 days (d) gestation (term=150d), pregnant Merino ewes (n=6, control; n=4, IUGR) underwent surgery, with general anesthesia induced by intravenous injection of diazepam (0.3 mg/kg) and ketamine (7 mg/kg) and maintained with inhalation of isoflurane (1-2%) in oxygen with post-operative antibiotics and analgesia, to implant vascular catheters in the maternal jugular vein, fetal femoral artery and vein as well as the amniotic cavity. At 126±1d, ewes underwent cardiovascular MRI assessment using a 3T Siemens Skyra system in both a normoxic and hyperoxic (100% O2) state under general anesthesia induced and maintained as above (isoflurane, 2.5-2.75%). MRI assessment was performed using phase contrast (PC) measurements of blood flow in major fetal and placental vessels including uterine arteries (UTAs), umbilical vein (UV), ductus venosus, ascending aorta (AAO), main pulmonary artery, branch pulmonary arteries (PAs), ductus arteriosus, common carotid arteries (CCAs), superior vena cava and descending aorta. Foramen ovale (FO) shunting was calculated by subtracting flow in PAs from AAO. All blood flow measures were indexed to fetal weight calculated from the 3D MRI acquisition of fetal volume (4). Results: MH significantly increased fetal arterial PaO2 (Control: 19.1±1.6 vs 22.7±1.4 mmHg; IUGR: 16.1±1.7 vs 21.4±2.6). IUGR fetuses had significantly reduced uterine artery blood flow in comparison to controls which did not change in response to MH. Acute MH significantly increased blood flow in the fetal PAs and decreased blood flow through the FO whilst other major vessels were unaltered. The data was analyzed using a two-way ANOVA (statistical significance, P<0.05). Conclusions: We used PC-MRI to perform a comprehensive assessment of the fetal circulation and show that acute MH increases PA and decreases FO blood flow in both controls and IUGR fetuses. Unaltered flow in the UV and CCAs with increased arterial fetal oxygen content suggests increased oxygen delivery to the fetus and the brain. Despite reduced UTAs blood flow, a chronic MH treatment can be of great benefit to an IUGR fetus to improve oxygen delivery, particularly to important organs like the brain, heart, lungs and liver that may help the timely development and maturation of its vital organs and improve its growth trajectory.

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