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. α-Adrenergic blockade resulted in a 22% decrease in blood pressure in the hypoxemic group, three times greater than the controls. Pre-hypoxemia α-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 α-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.
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