Parer J T
Am J Obstet Gynecol. 1984 Apr 15;148(8):1118-22. doi: 10.1016/0002-9378(84)90638-0.
To determine if vagal blockade during hypoxic bradycardia improves fetal oxygenation, 10 studies were carried out on five chronically instrumented sheep after 0.8 week of gestation. At a mean maternal arterial oxygen tension of 33 +/- 4 mm Hg, the fetal heart rate decreased 20% to 137 +/- 19 bpm, and fetal oxygen consumption decreased 42% to 4.6 +/- 1.5 ml/min/kg of fetus. After 200 micrograms atropine was infused into a fetal vein, fetal heart rate increased immediately to 249 +/- 26 bpm. Fetal oxygen consumption was unchanged. Fetal heart rate increased by 18 bpm after atropine in the normoxic fetus. These studies show that there is a substantial bradycardia due to an increase in vagal activity during hypoxia in the fetus and that blockade of this activity causes a marked tachycardia but no increase in fetal oxygen uptake.
为确定缺氧性心动过缓期间迷走神经阻滞是否能改善胎儿氧合，在妊娠0.8周后对五只长期植入仪器的绵羊进行了10项研究。在母体动脉血氧分压平均为33±4 mmHg时，胎儿心率下降20%，至137±19次/分，胎儿氧耗量下降42%，至4.6±1.5 ml/（min·kg胎儿体重）。向胎儿静脉注入200微克阿托品后，胎儿心率立即增至249±26次/分。胎儿氧耗量未变。在正常氧合胎儿中，注入阿托品后胎儿心率增加了18次/分。这些研究表明，胎儿在缺氧期间由于迷走神经活动增加而出现显著心动过缓，阻断这种活动会导致明显的心动过速，但胎儿氧摄取并未增加。
