Placental hypoxia is associated with maternal hypertension, placental insufficiency, and fetal growth restriction. In the pregnant guinea pig, prenatal hypoxia during early gestation inhibits cytotrophoblast invasion of spiral arteries, increases maternal blood pressure, and induces fetal growth restriction. In this study the impact of chronic maternal hypoxia on fetal heart structure was evaluated using four-dimensional echocardiography with spatiotemporal image correlation and tomographic ultrasound, and uterine and umbilical artery resistance/pulsatility indexes and fetal heart function were evaluated using pulsed-wave Doppler ultrasound. Pregnant guinea pigs were exposed to normoxia ( = 7) or hypoxia (10.5% O, = 9) at 28-30 days gestation, which was maintained until full term (65 days). At full term, fetal heart structure and outflow tracts were evaluated in the four-chamber view. Fetal heart diastolic function was assessed by E wave-to-A wave diastolic filling ratios (E/A ratios) of both ventricles and systolic function by the myocardial performance index (or Tie) of left ventricles of normoxic ( = 21) and hypoxic ( = 17) fetuses. There were no structural abnormalities in fetal hearts. However, hypoxia induced asymmetric fetal growth restriction and increased the placental/fetal weight compared with normoxic controls. Hypoxia increased Doppler resistance and pulsatility indexes in the uterine, but not umbilical, arteries, had no effect on the Tie index, and increased the E/A ratio in left, but not right, ventricles. Thus, prolonged hypoxia, starting at midgestation, increases uterine artery resistance and generates fetal growth restriction at full term. Furthermore, the enhanced cardiac diastolic filling with no changes in systolic function or umbilical artery resistance suggests that the fetal guinea pig systemic circulation undergoes a compensated, adaptive response to prolonged hypoxia exposure.

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Abstract: We hypothesized that the physiological adaptations of the fetus in response to chronic intrauterine hypoxia depend on its sex and the gestational age of exposure. Methods. Pregnant guinea pigs were exposed to room air (normoxia, NMX) or 10.5%O2 (hypoxia, HPX) at either 25d (Early Onset) or 50d (Late Onset) gestation until term (~65d). We evaluated the effects of hypoxia on hemodynamic and cardiac function indices using Doppler ultrasound (US) and determined sex-related differences in near-term fetuses. Indices of uterine/umbilical artery pulsatility (PI index) and fetal heart systolic and diastolic function (Tei index and E/A ratios, respectively) were measured in utero and fetal body (FBW) and organ weights measured from extracted fetuses. Results. Both early and late onset HPX decreased FBW in both males and females, had no effect on placenta wts, and increased placenta wt/FBW ratios. Early but not late onset HPX increased uterine artery PI but neither HPX condition affected umbilical artery PI. Early onset HPX increased left ventricle E/A ratios in both males and females while late onset HPX increased right ventricle E/A ratio in females only. Hypoxia had no effect on the Tie index in either sex. Conclusions: Early and late onset HPX induce placental insufficiency, fetal growth restriction, and increase diastolic filling depending on the sex, with female fetuses having a greater capacity than males to compensate to intrauterine hypoxia.

Facial clefts are among the most common congenital defects. Ultrasound (US) imaging of secondary fetal palate, especially the detection of isolated defects, remains challenging. Currently described two-dimensional (2D) and three-dimensional methods are technically demanding and impractical for application during routine fetal anatomy evaluation. As an adjunct method, magnetic resonance imaging can provide additional information but has its limitations. We present a novel 2D US approach using axial and sagittal planes to evaluate the fetal palate and demonstrate the main differences between an intact palate, isolated cleft palate, and a cleft lip with cleft palate.

Introduction. Studies indicate a very low rate of SARS-CoV-2 detection in the placenta or occasionally a low rate of vertical transmission in COVID-19 pregnancy. SARS-CoV-2 Delta variant has become a dominant strain over the world and possesses higher infectivity due to mutations in its spike receptor-binding motif. Case Presentation. To determine whether SARS-CoV-2 Delta variant has increased potential for placenta infection and vertical transmission, we analyzed SARS-CoV-2 infection in the placenta, umbilical cord, and fetal membrane from a case that unvaccinated mother and her neonate were COVID-19 positive. A 35-year-old primigravida with COVID-19 underwent an emergent cesarean delivery due to placental abruption in the setting of premature rupture of membranes. The neonate tested positive for SARS-CoV-2 within the first 24 hours, and then again on days of life 2, 6, 13, and 21. The placenta exhibited intervillositis, increased fibrin deposition, and syncytiotrophoblast necrosis. Sequencing of viral RNA from fixed placental tissue revealed SAR-CoV-2 B.1.167.2 (Delta) variant. Both spike protein and viral RNA were abundantly present in syncytiotrophoblasts, cytotrophoblasts, umbilical cord vascular endothelium, and fetal membranes. Discussion/Conclusion. We report with strong probability the first SARS-CoV-2 Delta variant transplacental transmission. Placental cells exhibited extensive apoptosis, senescence, and ferroptosis after SARS-CoV-2 Delta infection