Lewis A B, Donovan M, Platzker A C
Biol Neonate. 1980;37(5-6):233-42. doi: 10.1159/000241281.
The cardiovascular responses of 11 fetal lambs in utero to hypoxemia were evaluated before and after autonomic blockade. Hypoxemia was produced by lowering the maternally inspired oxygen or by progressive constriction of the umbilical cord by a cuff occluder. The animals were studied serially from 112 days' gestation to term. Fetal carotid arterial pO2 fell from 24 to 12 torr and was accompanied by a 35% decline in heart rate and 32% rise in blood pressure. Parasympathetic blockade with atropine produced a 114% increase in heart rate in the hypoxemic fetuses compared to 26% in the normoxemic controls. Pretreatment with atropine prevented the hypoxemia-induced bradycardia without altering the hypertensive response. alpha-Adrenergic blockade resulted in a 22% decrease in blood pressure in the hypoxemic group, three times greater than the controls. Pre-hypoxemia alpha-blockade prevented the hypertension without affecting the fall in fetal heart rate. It is concluded that fetal bradycardia in response to hypoxemia is due to a direct increase in parasympathetic activity rather than secondary to a hypertension-induced baroreflex. The alpha-mediated increase in systemic vascular resistance and blood pressure may be a compensatory mechanism to maintain placental blood flow despite the decline in combined ventricular output.
在自主神经阻滞前后，对11只子宫内胎羊对低氧血症的心血管反应进行了评估。低氧血症通过降低母体吸入的氧气或用袖带封堵器逐渐收缩脐带产生。从妊娠112天到足月对这些动物进行了系列研究。胎儿颈动脉血氧分压从24降至12托，并伴有心率下降35%和血压升高32%。与正常氧合对照组心率升高26%相比，用阿托品进行副交感神经阻滞使低氧血症胎儿的心率升高114%。用阿托品预处理可预防低氧血症诱导的心动过缓，而不改变高血压反应。α-肾上腺素能阻滞导致低氧血症组血压下降22%，是对照组的三倍。低氧血症前α-阻滞剂可预防高血压，而不影响胎儿心率下降。结论是，胎儿对低氧血症的心动过缓是由于副交感神经活动直接增加，而非继发于高血压诱导的压力反射。尽管心室联合输出量下降，但α介导的全身血管阻力和血压增加可能是维持胎盘血流的一种代偿机制。
