XXXX exposure during pregnancy persistently attenuates cranially directed blood flow in the developing fetus: evidence from ultrasound imaging in a @entity19 second trimester equivalent model.

@entity1032 @entity851 @entity167 @entity19 @entity26 @entity5161 @entity1068
BACKGROUND: @entity1068 ( @entity167 ) consumption during pregnancy can lead to fetal @entity851 , @entity1032 , and neurodevelopmental delay. The fetal brain initiates neurogenesis and vasculogenesis during the second trimester, and depends on maternal-fetal circulation for nutrition and growth signals. We used high-resolution in vivo ultrasound imaging to test the hypothesis that @entity167 interferes with fetal brain-directed blood flow during this critical developmental period. METHODS: Pregnant @entity19 were lightly anesthetized on gestational day 12 with an @entity5161 / @entity26 mixture. We assessed the effect of single and repeated binge-like maternal @entity167 exposures at 3 g/kg, administered by intragastric gavage or intraperitoneal injection, on maternal circulation and fetal umbilical, aortic, internal carotid, and middle cerebral arterial circulation. RESULTS: Binge maternal @entity167 exposure, regardless of exposure route, significantly reduced fetal arterial blood acceleration and velocity time integral (VTI), from umbilical to cerebral arteries, without a change in fetal heart rate and resistivity indices. Importantly a single maternal binge @entity167 exposure induced persistent suppression of fetal arterial VTI for at least 24 hours. Repeated binge episodes resulted in a continuing and persistent suppression of fetal VTI. Qualitative assessments showed that maternal @entity167 exposure induced oscillatory, nondirectional blood flow in fetal cerebral arteries. Maternal cardiac and other physiological parameters remained unaltered. CONCLUSIONS: These data show that binge-type maternal @entity167 exposure results in rapid and persistent loss of blood flow from the umbilical artery to the fetal brain, potentially compromising nutrition and the maternal/fetal endocrine environment during a critical period for neuron formation and angiogenesis in the maturing brain.
