Parer J T
Am J Obstet Gynecol. 1983 Nov 1;147(5):592-7. doi: 10.1016/0002-9378(83)90024-8.
To determine the importance of beta-adrenergic activity during hypoxia in the fetus, 13 studies were carried out on seven chronically instrumented sheep at nine tenths of gestation. Hypoxia was induced by having the mother breathe gas mixtures that resulted in a reduction of maternal arterial oxygen tension to 32 mm Hg. Hypoxia resulted in a decrease in fetal heart rate (165 +/- 17 to 140 +/- 28 bpm) and fetal oxygen consumption (5.9 +/- 1.3 to 3.0 +/- 1.5 ml/min/kg) and increases in fetal arterial and umbilical venous pressures. There was no change in umbilical blood flow (209 +/- 58 ml/min/kg). Propranolol, 1.1 ml/kg, was rapidly infused into a fetal vein to achieve complete beta-adrenergic blockade. Umbilical vascular resistance increased significantly, fetal heart rate decreased to 112 +/- 22 bpm, and umbilical blood flow decreased to 165 +/- 73 ml/min/kg. There was no further decrease in fetal oxygen consumption. These decreases are approximately twice those seen after propranolol without hypoxia. These findings suggest that during hypoxia there is an increase in beta-adrenergic activity, which tends to maintain fetal heart rate and umbilical blood flow. This activity counteracts the increase in vagal activity with hypoxia, which decreases heart rate.
为了确定胎儿缺氧期间β-肾上腺素能活性的重要性，对7只在妊娠十分之九个月时长期植入仪器的绵羊进行了13项研究。通过让母体呼吸导致母体动脉血氧分压降至32mmHg的混合气体来诱导缺氧。缺氧导致胎儿心率下降（从165±17次/分钟降至140±28次/分钟）、胎儿耗氧量下降（从5.9±1.3毫升/分钟/千克降至3.0±1.5毫升/分钟/千克），以及胎儿动脉压和脐静脉压升高。脐血流量没有变化（209±58毫升/分钟/千克）。将1.1毫升/千克的普萘洛尔快速注入胎儿静脉以实现完全的β-肾上腺素能阻断。脐血管阻力显著增加，胎儿心率降至112±22次/分钟，脐血流量降至165±73毫升/分钟/千克。胎儿耗氧量没有进一步下降。这些下降幅度约为无缺氧情况下普萘洛尔给药后下降幅度的两倍。这些发现表明，在缺氧期间β-肾上腺素能活性增加，这倾向于维持胎儿心率和脐血流量。这种活性抵消了缺氧时迷走神经活性的增加，而迷走神经活性增加会降低心率。
