Fowden A L, Ralph M M, Silver M
Dept. of Physiology, Monash University, Clayton, Victoria, Australia.
Exp Clin Endocrinol. 1994;102(3):212-21. doi: 10.1055/s-0029-1211285.
Prostaglandins (PGs) are produced by a variety of uteroplacental tissues during pregnancy and are released into the fetal fluid sacs and both the uterine and umbilical circulations. Uterine PG output increases towards term and is enhanced by maternal undernutrition in pregnant ewes and mares. In both species, withdrawal of food but not water for 30-48 h increases uterine venous PG levels and the uterine venous arterial concentration differences in PGE and 13, 14, dihydro-15-keto-prostaglandin F2 alpha (PGFM), the stable metabolite of PGF2 alpha. The increments in uterine V-A concentration differences in PGE and PGFM increase towards term and are associated with raised plasma PG levels in the fetal circulation. The PG changes observed during fasting are closely related to the fall in plasma glucose and the rise in plasma FFA in peripheral plasma. When normal metabolite levels are restored either by refeeding or glucose infusion, there is a rapid fall in PG levels with a narrowing of the uterine V-A concentration differences in the ewe and mare. When the data from all the animals are combined, there is an inverse correlation between uterine glucose uptake and PGFM output in both the pregnant ewe and mare. The availability of glucose and FFA to the gravid uterus therefore has an important role in controlling uteroplacental PG production and metabolism in late gestation although the specific steps in biochemical pathways regulated by these metabolites remain unclear. In the ewe, fasting increases uterine contractility and leads to early delivery of viable lambs in animals close to term (> 95% gestation), whereas in the mare it causes premature delivery of non-viable foals in most animals in late gestation (> 80% gestation). Nutritionally induced changes in uteroplacental PG production and metabolism therefore have important consequences for the outcome of pregnancy and may have a pivotal role in the induction of labour both before and at normal term.
前列腺素（PGs）在妊娠期间由多种子宫胎盘组织产生，并释放到胎儿囊液以及子宫和脐循环中。子宫PG的产量在足月时增加，并且在怀孕的母羊和母马中，母体营养不足会使其增加。在这两个物种中，禁食30 - 48小时但不禁水会增加子宫静脉PG水平以及PGE和13,14 - 二氢 - 15 - 酮 - 前列腺素F2α（PGFM，PGF2α的稳定代谢产物）的子宫静脉 - 动脉浓度差。PGE和PGFM的子宫V - A浓度差的增加在足月时增大，并与胎儿循环中血浆PG水平升高相关。禁食期间观察到的PG变化与外周血浆中血糖下降和血浆游离脂肪酸（FFA）升高密切相关。当通过重新喂食或输注葡萄糖恢复正常代谢物水平时，PG水平迅速下降，母羊和母马的子宫V - A浓度差缩小。当将所有动物的数据合并时，怀孕母羊和母马的子宫葡萄糖摄取与PGFM产量之间存在负相关。因此，尽管这些代谢物调节的生化途径中的具体步骤尚不清楚，但葡萄糖和FFA对妊娠子宫的可用性在控制妊娠晚期子宫胎盘PG的产生和代谢中具有重要作用。在母羊中，禁食会增加子宫收缩力，并导致接近足月（> 95%妊娠期）的动物早产活羔羊，而在母马中，禁食会导致大多数妊娠晚期（> 80%妊娠期）的动物早产未存活的驹。因此，营养诱导的子宫胎盘PG产生和代谢变化对妊娠结局具有重要影响，并且可能在足月前和足月时引产中起关键作用。
