Abstract
Delayed decelerations of fetal heart rate were produced by abruptly decreasing uterine blood flow to zero for 20 seconds in chronically instrumented, normoxic sheep. Fetal O2 content, and O2 tension in umbilical blood decreased significantly before the decline in heart rate. Fetal arterial blood pressure did not change significantly. Complete vagal blockade abolished the late deceleration and uncovered a late acceleration, which in turn was eliminated by total β-adrenergic blockade. We conclude that these late decelerations in normoxic sheep are vagally mediated and due to chemoreceptor rather than baroreceptor activity.
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