Brace R A
Am J Obstet Gynecol. 1986 Oct;155(4):889-93. doi: 10.1016/s0002-9378(86)80045-x.
The purpose of this study was to explore the effects of acute hypoxia on the volume of blood circulating in the fetus. The oxygen content of air inspired by chronically catheterized, near-term pregnant sheep was reduced and supplemented with carbon dioxide in an attempt to maintain fetal carbon dioxide tension constant. Control fetal arterial oxygen tension averaged 22.3 +/- 0.7 (SE) mm Hg. During a 30-minute hypoxic period, reductions in fetal arterial oxygen tension by 2.4 to 12.5 mm Hg in individual animals were associated with decreases in fetoplacental blood volume of 1.1% to 14.3%. On the average (n = 14), fetal blood volume decreased by 6.7% +/- 0.8% when oxygen tension decreased by 7.7 +/- 0.9 mm Hg. Both arterial and venous pressures increased significantly during the hypoxic period. Upon the return to breathing of room air, there was a transient overshoot of fetal PO2 of 1.0 +/- 0.4 mm Hg at 10 minutes, but fetal blood volume did not return to normal until 30 minutes after the hypoxia. Thus, the data suggest that acute fetal hypoxia causes rapid and sustained reductions in fetal blood volume whereas volume returns to normal only slowly after elimination of the hypoxia.
本研究的目的是探讨急性缺氧对胎儿循环血量的影响。对长期插管的近足月妊娠绵羊吸入的空气氧含量进行降低，并补充二氧化碳，以维持胎儿二氧化碳张力恒定。对照胎儿动脉氧分压平均为22.3±0.7（标准误）mmHg。在30分钟的缺氧期内，个别动物胎儿动脉氧分压降低2.4至12.5 mmHg，同时胎儿胎盘血量减少1.1%至14.3%。平均而言（n = 14），当氧分压降低7.7±0.9 mmHg时，胎儿血量减少6.7%±0.8%。缺氧期动脉压和静脉压均显著升高。恢复呼吸室内空气后，10分钟时胎儿PO2短暂超射1.0±0.4 mmHg，但胎儿血量直到缺氧后30分钟才恢复正常。因此，数据表明急性胎儿缺氧会导致胎儿血量迅速且持续减少，而缺氧消除后血量仅缓慢恢复正常。
