Kingdom J C, Kaufmann P
Department of Obstetrics and Gynaecology, University College London Medical School, UK.
Placenta. 1997 Nov;18(8):613-21; discussion 623-6. doi: 10.1016/s0143-4004(97)90000-x.
The increasing practice of preterm delivery in the fetal interest for conditions such as pre-eclampsia or intrauterine growth restriction (IUGR) has provided an opportunity to study placental structure in pregnancies with prenatal evidence of fetal compromise. These data suggest that the origin of fetal hypoxia in IUGR with absent end-diastolic flow in the umbilical arteries is due to a failure of oxygen transport from intervillous space to umbilical vein. Failure of the fetoplacental circulation to extract oxygen from the intervillous space under such circumstances means intervillous PO2 is closer to maternal arterial values than under physiological conditions. Correspondingly the placental villi are chronically exposed to a higher oxygen tension than under normal circumstances--the term ¿hyperoxia', relative to normal intraplacental oxygenation, is proposed to describe this situation. Both the trophoblast and villous core react to increased oxygen despite fetal hypoxia. These results challenge the generally accepted concept of ¿placental hypoxia' in all circumstances where fetal hypoxia might arise. Therefore three categories are proposed for the origins of fetal hypoxia: (1) preplacental hypoxia; (2) uteroplacental hypoxia; and (3) postplacental hypoxia. Examples for these three disease states are listed in this review and the structural reaction patterns of placental villi to these differences in oxygenation are discussed.
出于胎儿利益考虑，针对子痫前期或胎儿生长受限（IUGR）等情况越来越多地进行早产，这为研究产前有胎儿窘迫证据的妊娠中的胎盘结构提供了机会。这些数据表明，脐动脉舒张末期血流缺失的IUGR中胎儿缺氧的起源是由于氧从绒毛间隙向脐静脉转运失败。在这种情况下，胎儿-胎盘循环无法从绒毛间隙摄取氧气意味着绒毛间隙的氧分压比生理条件下更接近母体动脉值。相应地，胎盘绒毛长期暴露于比正常情况下更高的氧张力下——相对于正常胎盘内氧合，提出“高氧”一词来描述这种情况。尽管存在胎儿缺氧，但滋养层和绒毛核心对增加的氧气都有反应。这些结果挑战了在可能出现胎儿缺氧的所有情况下普遍接受的“胎盘缺氧”概念。因此，提出胎儿缺氧的起源分为三类：（1）胎盘前缺氧；（2）子宫胎盘缺氧；（3）胎盘后缺氧。本综述列出了这三种疾病状态的示例，并讨论了胎盘绒毛对这些氧合差异的结构反应模式。
