Placental Gas Exchange and the Oxygen Supply to the Fetus

Abstract

The oxygen supply of the fetus depends on the blood oxygen content and flow rate in the uterine and umbilical arteries and the diffusing capacity of the placenta. Oxygen consumption by the placenta is a significant factor and a potential limitation on availability to the fetus. The relevance of these several factors as well as responses to acute or sustained hypoxia has been explored in the sheep model. In addition, much has been learned in the context of hypobaric hypoxia by studying human populations that have resided at high altitude for varying periods of time. Embryonic development occurs under anaerobic conditions and even the fetus is adapted to a low oxygen environment. Nevertheless, there is a reserve capacity, and during acute hypoxia the fetus can counter a 50% reduction in oxygen delivery by increasing fractional extraction. During sustained hypoxia, on the other hand, fetal growth is slowed, although oxygen consumption is unaltered when corrected for fetal mass. Similarly, birth weight is reduced in humans living at high altitude even if the effect is tempered in those with a long highland ancestry. Placental mass changes little during sustained hypoxia in sheep or humans at high altitude. This conceals the fact that there are structural changes and that placental oxygen consumption is reduced. The underlying mechanisms are a current focus of research. One intriguing possibility is that increased anaerobic metabolism of glucose in the placenta spares oxygen for the fetus but reduces its supply of substrate and thereby limits fetal growth.

In Vivo Quantification of Placental Insufficiency by BOLD MRI: A Human Study

“…This is particularly interesting, given that the placenta consumes a significant amount of oxygen with normal term placenta, more than 40% of the overall oxygen delivered to uterus 30, 31 . One possibility is that in pathological placentas, the rate of oxygen consumption may not remain constant.…”

The neutrophil‐lymphocyte ratio is prognostic in patients with early stage aggressive peripheral T cell lymphoma

“…There were no between-group differences in fetal oxygen saturation and extraction. This relative stability of fetal SaO2 in infants of SCD-affected women may be secondary to high fetal-blood oxygen-affinity (promoting transplacental oxygen transfer) (Carter, 2015) and lower maternal-blood oxygen affinity of sickle haemoglobin compared to normal haemoglobin (altered Bohr Effect), resulting in marked liberation of oxygen from maternal cells, particularly at pH<7Á4 (Ueda et al, 1979). Yet, preservation of fetal oxygenation in this manner may come at the expense of increased maternal sickling, given the propensity for sickle haemoglobin formation in de-oxygenated states (Ueda et al, 1979).…”

“…maternal anaemia) (Kingdom & Kaufmann, 1997). Although during short-term response to maternal anaemia, uterine blood flow remains unaltered, uterine oxygen delivery is hardly reduced, and uterine/placental/fetal oxygen-consumption is negligibly lower (Carter, 2015), thus maintaining high placental oxygen-consumption; during long-term hypoxic conditions, placental oxygen-consumption falls, promoting fetal oxygen availability (Carter, 2015). Thus, the lack of difference in oxygen saturation/extraction between study groups potentially stems from the relative maintenance of adaptive capacities of feto-placental oxygen exchange and absence of acute-onset, severe maternal anaemia, while diminished fetal growth velocities in SCD-affected women probably reflect subtle, ongoing, long-term hypoxic insults (Carter, 2015).…”

Maternal plasma angiogenic index-1 (placental growth factor/soluble vascular endothelial growth factor receptor-1) is a biomarker for the burden of placental lesions consistent with uteroplacental underperfusion: a longitudinal case-cohort study

“…Physiologic transformation of the spiral arteries increases the size of these vessels, allowing blood to flow into the intervillous space [15–22], where oxygen and nutrients are transported to the fetus [23–26]. Disruption of maternal vascular development is thought to result in reduced blood supply to the placenta.…”