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circulation. We sought to evaluate changes in the pulmonary artery doppler following maternal hyperoxygenation in utero, during the third trimester of pregnancy. STUDY DESIGN: Forty six women with a singleton gestation greater than or equal to 31 weeks gestational age were prospectively recruited to the study. A fetal echocardiogram was performed on all subjects to exclude congenital heart disease. Pulsatility index (PI), Resistance index (RI), Peak systolic (PSV) and end diastolic velocity (EDV), acceleration time (AT), and ejection time (ET) were taken within the proximal portion of the fetal main pulmonary artery (PA). AT:ETwas used to assess pulmonary vascular resistance (PVR). Doppler measurements were taken at baseline and repeated immediately following maternal hyperoxygenation for 10 minutes (O2 100% v/v inhalational gas) at a rate of 12L/min via a partial nonrebreather mask. Doppler waveform measurements were also taken of the umbilical artery (UAD), middle cerebral artery (MCA) and the ductus arteriosus (DA). RESULTS: The median gestational age was 35 [33 e 37] weeks. There was a decrease in fetal PA PI following maternal hyperoxygenation (from 2.37 [2.04 e 2.70] to 2.05 [1.69 e 2.41], p1⁄40.001). The resistance index of the PA decreased from (0.86 [0.810.91] to 0.78 [0.69-0.87]. There was an increase in PA AT (57 [42-71] to 66 [49 e 82] ms, leading to an increase in AT:ET following maternal hyperoxygenation (0.32 to 0.34], p1⁄40.001) (Table 1). There were no significant changes in the resistance indices of the UAD and DA. There was a significant increase in MCA blood flow, but not in MCA resistance indices. CONCLUSION: Maternal hyperoxygenation offers the opportunity to assess the reactivity of the pulmonary vasculature before birth. Our findings would indicate a reduction in fetal pulmonary vascular resistance with secondary increased fetal pulmonary blood flow. This was not achieved at the expense of ductal constriction. There was evidence of improved MCA peak systolic velocity parameters; this was likely due to the positive impact of improved pulmonary venous return on left ventricular preload. The hyperoxygenation test can inform us of functional rather than anatomical information in relation to the pulmonary arteries and this warrants further exploration in a larger cohort.