摘要翻译：
胎儿的氧气输送和消耗以及血气与胎龄的关系。氧通过扩散穿过胎盘，胎盘通透性高。因此，胎儿接受足够的量，但血管PO$_2$比出生后低得多。对胎儿持续低氧血症和急性40-45%出血的研究表明，低氧血症是不可耐受的，而出血是不可耐受的。这表明，如果胎儿PO2$明显下降，则O2$从血液向组织的扩散受到损害。子宫血和脐血流量/胎儿体重随着妊娠的推进而逐渐下降。这导致胎儿低氧血症，增加PCO$_2$，降低pH。这减少了胎儿的O$_2$分娩，在胎儿羔羊和马中，胎儿的O$_2$消耗也减少了。O$_2$需求的减少与胎儿呼吸、身体运动和生长速度的减少有关。胎儿运动能力的下降是由于胎血浆PGE2浓度的升高，在绵羊中，胎血浆PGE2浓度从120天开始升高，是由于产前胎儿皮质醇的升高。此外，给胎羊腺苷使胎儿呼吸和快速眼动睡眠减少，血浆腺苷浓度在妊娠晚期增加。胎儿血浆中抑制胎儿运动的神经类固醇水平随着妊娠的推进而增加。产前皮质醇升高也抑制胎儿生长。在正常妊娠中，这些机制有效地运行，以维持胎儿氧气消耗和分娩之间的适当平衡。然而，在进一步减少O2$分娩或增加胎儿O2$需求的妊娠中，O2$分娩与消耗之间的不匹配可能会加剧，导致IUGR、缺氧器官损害或死胎。
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英文标题：
《Fetal oxygen delivery and consumption and blood gases in relation to
  gestational age》
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作者：
D.W. Rurak, M.Y. Shen and K.S. Joseph
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最新提交年份：
2021
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分类信息：

一级分类：Quantitative Biology        数量生物学
二级分类：Other Quantitative Biology        其他定量生物学
分类描述：Work in quantitative biology that does not fit into the other q-bio classifications
不适合其他q-bio分类的定量生物学工作
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英文摘要：
  Fetal oxygen delivery and consumption and blood gases in relation to gestational age. Oxygen crosses the placenta by diffusion and placental permeability to O$_2$ is high. Thus, the fetus receives adequate amounts, but vascular Po$_2$ is much lower than after birth. Studies of sustained fetal hypoxemia and acute 40-45% hemorrhage show that hypoxemia is not tolerated whereas hemorrhage is. This suggests that if fetal Po$_2$ falls markedly, O$_2$ diffusion from blood to tissue is impaired. Uterine blood and umbilical blood flows/fetal weight fall progressively with advancing gestation. This results in fetal hypoxemia, an increase in Pco$_2$, and decrease in pH. This decreases fetal O$_2$ delivery, and in fetal lambs and horses there is a decrease in fetal O$_2$ consumption. The decrease in O$_2$ demands is linked to a decrease in fetal breathing and body movements and growth rate. The decrease in fetal motility is due to an increase in fetal plasma PGE2 concentration, which begins at ~120 days GA in sheep and is due to the prepartum rise in fetal cortisol. Also, adenosine administration to fetal lambs decreases fetal breathing and REM sleep and the plasma adenosine concentration increases in late gestation. The fetal plasma levels of neurosteroids, which suppress fetal motility, increase with advancing gestation. The prepartum cortisol rise also inhibits fetal growth. In normal pregnancies, these mechanisms operate effectively to maintain an appropriate balance between fetal oxygen consumption and delivery. However, in pregnancies with either further reduce O$_2$ delivery or increase fetal O$_2$ demands, the mismatch between O$_2$ delivery and consumption may worsen leading to IUGR, hypoxic organ damage or stillbirth.
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PDF链接：
https://arxiv.org/pdf/2109.11616