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.