Howard R B, Hosokawa T, Maguire M H
Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66103.
Am J Obstet Gynecol. 1987 Nov;157(5):1261-6. doi: 10.1016/s0002-9378(87)80307-1.
Effects of maternal hypoxia on fetoplacental vascular resistance in the human placenta were investigated in an in vitro model in which single anatomic subunits (cotyledons) from term placentas were perfused at constant flow through both fetal and maternal circuits by means of a physiologic salt solution containing dextran. Acute reduction of oxygen tension in the maternal perfusate induced prompt fetoplacental vasoconstriction that recovered rapidly on restoration of oxygen to the perfusate. The response, hypoxic fetoplacental vasoconstriction, could be repeatedly demonstrated in the same cotyledon. The time course of hypoxic fetoplacental vasoconstriction was inversely related to oxygen tension of maternal arterial and maternal and fetal venous perfusates. Maternal and fetal venous perfusate pH and PCO2 did not change during the response. It is concluded that hypoxic fetoplacental vasoconstriction is triggered by decreased oxygen availability. It is suggested that hypoxic fetoplacental vasoconstriction may play a role in local regulation of human fetoplacental blood flow in vivo and may contribute to poor fetal prognosis in preeclampsia.
在一个体外模型中研究了母体缺氧对人胎盘胎儿 - 胎盘血管阻力的影响，该模型中，足月胎盘的单个解剖亚单位（小叶）通过含有右旋糖酐的生理盐溶液以恒定流量通过胎儿和母体循环进行灌注。母体灌注液中氧张力的急性降低会引起迅速的胎儿 - 胎盘血管收缩，当灌注液恢复氧气后，血管收缩迅速恢复。这种反应，即缺氧性胎儿 - 胎盘血管收缩，可在同一小叶中反复证明。缺氧性胎儿 - 胎盘血管收缩的时间进程与母体动脉、母体和胎儿静脉灌注液的氧张力呈负相关。在反应过程中，母体和胎儿静脉灌注液的pH值和PCO2没有变化。得出的结论是，缺氧性胎儿 - 胎盘血管收缩是由氧气供应减少引发的。有人提出，缺氧性胎儿 - 胎盘血管收缩可能在体内人胎儿 - 胎盘血流的局部调节中起作用，并且可能导致子痫前期中不良的胎儿预后。
