Department of Obstetrics and Gynecology, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
Department of Obstetrics and Gynecology, St. George's Hospital, London, United Kingdom; Women's Health & Perinatal Research Group, Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
Placenta. 2020 Jan 15;90:103-108. doi: 10.1016/j.placenta.2019.12.014. Epub 2019 Dec 16.
We hypothesized that nifedipine and sildenafil would have no detrimental effects on placental hemodynamics and gas exchange under fetal hypoxemia.
In 33 chronically instrumented fetal sheep, placental volume blood flow (Q) and umbilical artery (UA) vascular impedance were measured by Doppler ultrasonography. Fetal carotid artery blood pressure and blood gas values were monitored. After baseline data collection, maternal and fetal hypoxemia were induced. Following hypoxemia phase data collection, 12 fetuses received sildenafil and 9 fetuses nifedipine infusion, and 12 fetuses served as controls receiving saline infusion. Data were collected 30 and 120 min after infusion was started. Then maternal oxygenation was normalized and normoxemia phase data were collected, while infusion was continued.
Hypoxemia significantly decreased fetal pO and blood pressure. In the sildenafil group at 30- and 120-min hypoxemia + infusion phases, fetal blood pressure and Q were significantly lower and pCO higher than at baseline without returning to baseline level at normoxemia + infusion phase. In hypoxemia, nifedipine did not affect fetal blood pressure or placental hemodynamics. Both in the sildenafil and nifedipine groups, fetal pO remained significantly lower at normoxemia + infusion phase than in the control group. Umbilical artery vascular impedance did not change during the experiment.
In fetal hypoxemia, sildenafil had detrimental effects on placental hemodynamics that disturbed placental gas exchange. Nifedipine did not alter placental hemodynamics in hypoxemia but disturbed placental gas exchange upon returning to normoxemia. Umbilical artery vascular impedance did not reflect alterations in placental hemodynamics.
我们假设硝苯地平和西地那非在胎儿低氧血症下不会对胎盘血液动力学和气体交换产生不利影响。
在 33 只慢性仪器化胎儿羊中，通过多普勒超声测量胎盘容积血流量（Q）和脐动脉（UA）血管阻抗。监测胎儿颈动脉血压和血气值。在基线数据收集后，诱导母体和胎儿低氧血症。在低氧血症阶段数据收集后，12 只胎儿接受西地那非输注，9 只胎儿接受硝苯地平输注，12 只胎儿作为接受生理盐水输注的对照。在开始输注后 30 和 120 分钟收集数据。然后使母体氧合正常化并收集正常氧合阶段的数据，同时继续输注。
低氧血症显著降低了胎儿的 pO 和血压。在西地那非组，在 30 分钟和 120 分钟的低氧血症+输注阶段，胎儿血压和 Q 明显低于基线值，而 pCO 高于基线值，在正常氧合+输注阶段并未恢复到基线水平。在低氧血症时，硝苯地平不影响胎儿血压或胎盘血液动力学。在西地那非和硝苯地平组中，胎儿 pO 在正常氧合+输注阶段均显著低于对照组。在整个实验过程中，脐动脉血管阻抗没有变化。
在胎儿低氧血症中，西地那非对胎盘血液动力学产生有害影响，扰乱了胎盘气体交换。硝苯地平在低氧血症时不会改变胎盘血液动力学，但在恢复到正常氧合时会干扰胎盘气体交换。脐动脉血管阻抗不能反映胎盘血液动力学的变化。
