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Effect of uterine hypercontractility on the placenta and the fetal brain
Abstract Number: BP-6
Abstract Type: Original Research
Introduction: Synthetic oxytocin (OXT) for induction and augmentation of labor is associated with a 4-fold increase in uterine hypercontractility, including tetanic uterine contraction. Placental perfusion is profoundly impaired during such events, but whether this has any effect on the developing fetus remains unstudied. Here, in a term pregnant rat model, we tested the hypothesis that OXT-induced uterine hypercontractility causes placental hypoxia and induces oxidative stress in the fetal brain.
Methods: Placental perfusion and oxygenation were assessed in gestational day 21 pregnant SD rats pre- and post- 100 mcg/kg OXT in an Agilent/Varian 4.7 T MRI scanner (n = 2). Perfusion was quantified with dynamic contrast-enhanced MRI using the initial area under the curve (AUC) approach and washout slope of the DCE time-intensity curve. Placental oxygenation and deoxyhemoglobin concentration were assessed by repeating placental R1 and R2* measurements. To assess the effect on the placental and fetal brain transcriptome, RNA was isolated from the labyrinthine zone of the placenta and the right fetal cerebral cortex 24 h after either OXT or saline for RNA-seq analysis (n = 5 each). RNA-seq reads were aligned to the Ensembl top-level assembly with STAR version 2.0.4b and analyzed as described in the accompanying Figure Legend.
Results: Placental uptake of Dotarem® contrast was 30% slower post-OXT, indicating decreased blood flow (Fig 1). Placental R1 relaxation rate constant, reflecting tissue oxygen concentration, appeared unchanged by the administration of OXT. In contrast, the average placental R2*, reflecting deoxyHb concentration, increased from 34 ± 6 to 50 ± 30 s-1 (p = 0.02), though with significant location-dependent heterogeneity, suggesting lower placental oxygen saturation after OXT (Fig 2). RNA-seq analysis of the placental transcriptome showed a significant difference in expression of hypoxia-related genes after OXT treatment (Fig 3). In the fetal brain, OXT was associated with significant upregulation of mitochondrial genes mediating oxidative phosphorylation (Fig 4) suggestive for acute mitochondrial dysfunction.
Conclusion: Our data suggest that OXT-induced uterine hypercontractility can impair placental perfusion, induce hypoxia, and activate oxidative stress pathways in the fetal brain. Given the role of oxidative stress in neurodevelopmental disorders, our results provide a solid preclinical foundation for targeted clinical studies.