Placental Oxygen Consumption. Part I: In Vivo Studies—A Review

Abstract

At term of pregnancy, oxygen consumption by the human or ovine placenta accounts for 40 per cent of total oxygen uptake by the gravid uterus. In the sheep, most oxygen is used for oxidative phosphorylation of glucose; the remainder is probably utilized for non-mitochondrial processes. The ATP yield is expended mainly in protein synthesis and cation transport. The fractional 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 the Na+–K+-pump probably accounts for 20–30 per cent of oxygen uptake, with a smaller contribution from Ca2+-ATPase. Placental oxygen uptake remains constant during acute reductions in uterine oxygen supply and is maintained at the expense of the fetus. In the longer term, in experimental models of fetal growth restriction, placental oxygen consumption is reduced to a greater extent than fetal oxygen consumption. Placental oxygen consumption is greatly reduced under in vitro experimental conditions, due largely to an inadequate oxygen supply. This results in reduced protein synthesis and possibly inhibition of Na+–K+-ATPase. However, if the placenta is subjected to hyperoxia, by raising the Po2of the medium, there is an increase in anaerobic glycolysis and structural damage may ensue. Premature exposure of trophoblast 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 fetal growth and oxygen consumption.