Placental oxygen consumption. Part I: In vivo studies - A review

Authors
Citation
Am. Carter, Placental oxygen consumption. Part I: In vivo studies - A review, PLACENTA, 21, 2000, pp. S31-S37
Citations number
43
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
PLACENTA
ISSN journal
01434004 → ACNP
Volume
21
Year of publication
2000
Supplement
A
Pages
S31 - S37
Database
ISI
SICI code
0143-4004(200003/04)21:<S31:POCPII>2.0.ZU;2-G
Abstract
At term of pregnancy, oxygen consumption by the human or ovine placenta acc ounts for 40 per cent of total oxygen uptake by the gravid uterus. In the s heep, most oxygen is used for oxidative phosphorylation of glucose; the rem ainder is probably utilized for non-mitochondrial processes. The ATP yield is expended mainly in protein synthesis and cation transport. The fractiona l protein synthesis rate of ovine placenta is 60 per cent per day. Applying these data to man, protein synthesis is estimated to account for about 30 per cent of placental oxygen uptake. Probably this reflects the high rates of synthesis of peptide and steroid hormones. The Na+ gradient is the basis for secondary active transport of amino acids and other substances, and th e Na+-K+-pump probably accounts for 20-30 per cent of oxygen uptake, with a smaller contribution from Ca2+-ATPase. Placental oxygen uptake remains con stant during acute reductions in uterine oxygen supply and is maintained at the expense of the fetus. In the longer term, in experimental models of fe tal growth restriction, placental oxygen consumption is reduced to a greate r extent than fetal oxygen consumption. Placental oxygen consumption is gre atly reduced under in vitro experimental conditions, due largely to an inad equate oxygen supply. This results in reduced protein synthesis and possibl y inhibition of Na+-K+-ATPase. However, if the placenta is subjected to hyp eroxia, by raising the PO2 of the medium, there is an increase in anaerobic glycolysis and structural damage may ensue. Premature exposure of trophobl ast to high oxygen tensions in vivo may result in reduced villous branching , but this is likely to be a cause, rather than a consequence, of reduced f etal growth and oxygen consumption. (C) 2000 IFPA and Harcourt Publishers L td.