Fetal oxygen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep.
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 consumption, 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 beta-adrenergic blockade. We conclude that these late decelerations in normoxic sheep are vagally mediated and due to chemoreceptor rather than baroreceptor activity.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005318:Fetal Heart / Q000502:physiology*; D005333:Fetus / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D011433:Propranolol / Q000494:pharmacology; D012039:Regional Blood Flow; D012756:Sheep; D014599:Uterus / Q000098:blood supply*
D001285:Atropine; D011433:Propranolol; D010100:Oxygen