Placental oxygen consumption. Part I: In vivo studies - A review
Placental oxygen consumption. Part I: In vivo studies - A review
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DOI：
10.1053/plac.1999.0513
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发表时间：
2000-03-01
期刊：
影响因子：
3.8
通讯作者：
Carter, AM
中科院分区：
文献类型：
--
作者：
Carter, AM
在怀孕期间，人或羊胎盘的耗氧量占妊娠子宫总耗氧量的40%。在绵羊体内，大部分氧气用于葡萄糖的氧化磷酸化；其余的可能用于非线粒体过程。ATP产量主要用于蛋白质合成和阳离子转运。绵羊胎盘的蛋白质合成率为每天60%。将这些数据应用于男性，估计蛋白质合成约占胎盘摄氧量的30%。这可能反映了多肽和类固醇激素的高合成率。Na+梯度是氨基酸和其他物质二次主动转运的基础，Na+-K+泵可能占摄氧量的20-30%，而Ca~(2+)-ATPase的贡献较小。胎盘摄氧量在子宫供氧急剧减少期间保持不变，并以胎儿为代价维持。从长远来看，在胎儿生长受限的实验模型中，胎盘耗氧量比胎儿耗氧量减少的程度更大。在体外实验条件下，胎盘的耗氧量大大减少，这主要是由于氧气供应不足。这会导致蛋白质合成减少，并可能抑制Na+-K+-ATPase。然而，如果胎盘受到高氧的影响，通过提高介质中的PO2，就会增加厌氧糖酵解，从而可能导致结构损伤。在体内过早地将滋养细胞暴露在高氧压力下可能会导致绒毛分枝减少，但这可能是导致胎儿生长和氧气消耗减少的原因，而不是结果。(C)2000年IFPA和哈考特出版有限公司。
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 PO2 of 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. (C) 2000 IFPA and Harcourt Publishers Ltd.