Owens P C, Owens J A, Lovelock M, Chan E C, Falconer J, Robinson J S, Smith R
Faculty of Medicine, University of Newcastle, Shortland, New South Wales, Australia.
J Dev Physiol. 1989 Feb;11(2):63-71.
The opioid polypeptide beta-endorphin is present in fetal blood but it is not clear whether its source is the fetus or the placenta. We therefore measured beta-endorphin in extracts of fetal femoral arterial and umbilical venous blood plasma in sheep by radioimmunoassay to determine whether the fetus or the placenta is the major source of beta-endorphin in the fetal circulation. Chromatographic analysis of extracts of fetal arterial plasma showed that beta-lipotropin and other precursors of beta-endorphin made only a minor contribution to the immunoreactivity detected. Concentrations of immunoreactive beta-endorphin were higher in the femoral artery than in the umbilical vein in fetal sheep between 113 and 128 days of pregnancy. Therefore the placenta removes beta-endorphin or a closely related polypeptide of fetal origin from the umbilical circulation in sheep at this stage of gestation. Acute hypoxaemia and hypoglycaemia increase the concentrations of immunoassayable beta-endorphin in blood plasma of adult and fetal sheep, but little is known about the effects of chronic hypoxaemia or hypoglycaemia on the circulating levels of beta-endorphin and related polypeptides in the fetus. Therefore we also measured immunoreactive beta-endorphin in blood plasma from fetal sheep in which growth retardation in association with restricted placental growth was produced by removal of endometrial caruncles before mating. Intra-uterine growth retardation was accompanied by chronic hypoglycaemia and chronic hypoxaemia in the fetuses. This was not associated with higher concentrations of beta-endorphin-like immunoreactivity in fetal arterial or umbilical venous plasma, but was accompanied by significantly increased placental extraction of fetal immunoreactive beta-endorphin from the umbilical circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
阿片样多肽β-内啡肽存在于胎儿血液中，但尚不清楚其来源是胎儿还是胎盘。因此，我们通过放射免疫分析法测定了绵羊胎儿股动脉和脐静脉血浆提取物中的β-内啡肽，以确定胎儿循环中β-内啡肽的主要来源是胎儿还是胎盘。对胎儿动脉血浆提取物的色谱分析表明，β-促脂素和β-内啡肽的其他前体对检测到的免疫反应性贡献很小。在妊娠113至128天之间，绵羊胎儿股动脉中免疫反应性β-内啡肽的浓度高于脐静脉。因此，在妊娠的这个阶段，胎盘会从绵羊的脐循环中去除β-内啡肽或一种密切相关的胎儿源性多肽。急性低氧血症和低血糖会增加成年和胎儿绵羊血浆中可通过免疫测定的β-内啡肽浓度，但关于慢性低氧血症或低血糖对胎儿循环中β-内啡肽和相关多肽水平的影响知之甚少。因此，我们还测量了在交配前切除子宫内膜肉阜导致胎盘生长受限并伴有生长迟缓的绵羊胎儿血浆中的免疫反应性β-内啡肽。胎儿宫内生长迟缓伴有慢性低血糖和慢性低氧血症。这与胎儿动脉或脐静脉血浆中β-内啡肽样免疫反应性浓度升高无关，但伴有胎盘从脐循环中提取胎儿免疫反应性β-内啡肽的显著增加。（摘要截短于250字）
