Measuring Placental Oxygenation in a Rat Model of Intrauterine Growth Restriction (IUGR): Investigations with In-Vivo Magnetic Resonance Imaging (MRI).

INTRODUCTION: Optimal placental function is critical for appropriate fetal development and health outcomes. Understanding how in-vivo placental oxygen transfer aligns with placental vascular morphology and fetal growth is crucial for developing future diagnostic approaches. Substantial evidence exists on the detrimental effect of glucocorticoids causing IUGR and disruption in placental vasculature. However, the effects of glucocorticoids on in-vivo placental function remains less well understood. OBJECTIVE: This study aimed to examine whether in-vivo MRI methods can be used to detect changes in placental oxygenation in our well-established rat model of reduced placental vascularization and fetal growth. METHODS: 20 time-mated Wistar rats were administered with either vehicle or 0.5 μg/ml dexamethasone acetate (DEX), via drinking water from embryonic day (E) 13 until the end of the experiment. The dams were scanned serially at E15, E18 and E21 using 9.4 T MRI using a 3D multi-gradient-echo sequence with an oxygen-challenge paradigm to obtain 3D maps of the T2* MR signal relaxation time constant, which provides insight on placental oxygenation. T2* maps were calculated using the CRSI algorithm for manually defined regions of interest with custom Matlab software. Dams were then euthanized for tissue collection and the number and ordering of feto-placental units confirmed. Fetal and placental growth were assessed using weight and morphometric measures. RESULTS: Maternal DEX treatment significantly reduced fetal (-14.09%; p<0.0002), whole placental (-34.12%; p<0.0001), labyrinth placental (-30.31%; p<0.0001), and junctional placental (-41.98%; p<0.0001) weights. Preliminary analysis of the MRI data at E21 shows that placental T2* is decreased in DEX treated animals relative to controls, indicating reduced blood oxygenation. Ongoing analyses are determining whether these changes are dynamic across gestation. CONCLUSION: Our data confirms that maternal DEX treatment impairs fetal and placental growth. Importantly, these outcomes correspond with decreased placental oxygenation at E21 highlighting that our MRI methodology may be a useful tool for assessing how placental oxygenation corresponds with placental and fetal outcomes. Further analyses are on-going to determine how the MRI outcomes correlate across gestation with placental vascular structure, including investigation of additional metrics available from MRI. The results of this proof-of-concept study are promising and demonstrate the applicability of non-invasive MRI to investigate in-vivo placental function in a model of reduced placental vascularisation and fetal growth.