BOLD-MRI demonstrates acute placental and fetal organ hypoperfusion with fetal brain sparing during hypercapnia

Introduction We evaluated changes in placental and fetal hemodynamics in rodents during acute hypercapnia using BOLD-MRI and Doppler ultrasound. Methods Animals were anesthetized with pentobarbital and, in consecutive 4-min periods, breathed: air, 21%O2:5%CO2, and 95%O2:5%CO2. BOLD-MRI: Pregnant ICR mice (n = 6; E17.5) were scanned in a 4.7-T Bruker Biospec spectrometer. Placenta and fetal liver, heart and brain were identified on True-FISP images. Percent change in signal intensity (SI) were analyzed every 30 s from T2*-weighted GE images (TR/TE = 147/10 ms). Doppler: Pregnant Wistar rats (n = 6; E18-20) were anesthetized with pentobarbital and received abdominal Doppler ultrasound. Umbilical artery pulsatility index (PI) and fetal heart rate were assessed at baseline and after two minutes of both hypercapnic challenges. Results BOLD-MRI: Normoxic-hypercapnia caused immediate marked reduction in SI in placenta (−44% ± 5.5; p < 0.001), fetal liver (−32% ± 6.4; p < 0.001) and fetal heart (−53% ± 9.9; p < 0.001) but only minor changes in fetal brain (−13% ± 3.4; p < 0.01), suggesting fetal brain sparing. Doppler: Normoxic-hypercapnia caused a marked increase in umbilical artery PI (+27.4% ± 7.2; p < 0.001) and a reduction in fetal heart rate (−48 bpm; 95%CI -9.3 to −87.0; p = 0.02), suggesting acute fetal asphyxia. Conclusions Brief maternal hypercapnic challenge caused BOLD-MRI changes consistent with acute placental and fetal hypoperfusion with fetal brain sparing. The same challenge caused increased umbilical artery PI and fetal bradycardia on Doppler ultrasound, suggestive for acute fetal asphyxia. BOLD-MRI may be a suitable noninvasive imaging strategy to assess placental and fetal organ hemodynamics.