Adequate placental function is essential for the growth and development of a healthy fetus. A major cause of abnormal placental function is thought to occur from inadequate maternal spiral artery remodelling, leading to maternal vascular malperfusion (MVM) of the placenta and ultimately fetal growth restriction (FGR) and stillbirth due to uteroplacental hypoxia. Current methods of investigating a pregnancy at risk of FGR rely on ultrasound estimations of fetal size and Doppler studies. A more informative measure may be to quantify placental function in-vivo. Magnetic resonance imaging (MRI) has the ability to assess placental oxygen saturation (sO2), using Blood Oxygen-Level Dependent (BOLD), and the partial pressure of oxygen (pO2) using Oxygen-Enhanced MRI (OE MRI). These MRI techniques have been shown to correlate with gestation and poor pregnancy outcomes in cross sectional studies. MRI measures of placental oxygenation are hypothesised to be a potential antenatal tool for the identification and stratification of high risk pregnancies at risk of FGR related to uteroplacental hypoxia. To address this hypothesis changes in placental oxygenation, following maternal hyperoxia, were calculated in normal and FGR pregnancies in a cross sectional study. The change in placental oxygenation was reproduced longitudinally to determine if the rate of change differed between normal and FGR pregnancies. Baseline placental MRI parameters (R1 and R2*) and measures of the change in oxygenation were incorporated into a diagnostic model to identify FGR related to uteroplacental hypoxia, which was provisionally tested in a group of high risk pregnancies to demonstrate its potential clinical utility. Placental measures of baseline R1 and R2* were significantly increased in FGR pregnancies. The change in placental pO2 following hyperoxia was found to be significantly lower in FGR pregnancies. The change in pO2 declined similarly with gestation in both cross sectional and longitudinal studies, in normal and FGR pregnancies. There were no significant correlations in the change in placental sO2 with gestation or pregnancy outcome. The use of a diagnostic model combining baseline R1 and R2* and pO2 measures identified FGR with a high specificity, and provided additional information to aid in disease stratification and decision making in a significant proportion of the high risk pregnancies tested. In conclusion, MRI parameters of placental pO2 following hyperoxia are significantly lower in FGR pregnancies, in keeping with the concept of uteroplacental hypoxia. MRI techniques show promise in the identification of FGR pregnancies related to MVM through measures of placental function, irrespective of fetal size, and may aid in the disease stratification of high risk pregnancies.