Abstract
Acute studies of the role of aortic (AC) and carotid (CC) chemoreceptors in fetal circulatory regulation have been inconclusive. We measured heart rate (HR) and aortic pressure in 26 chronically instrumented fetal lambs (116-130 days) 2 to 5 days after surgery. Fourteen fetuses served as control, 7 had aortic and carotid (sinoaortic) denervation (SAD), and 5 had only carotid denervation. Acute hypoxia was produced for 20 sec by decreasing uterine blood flow by inflating a balloon in the maternal aorta. In the controls, hypoxia caused a 27% fall of HR (172±14 vs. 125±28 bpm, p<0.001) and an increase in aortic pressure (42.6±2.8 vs. 46.5±3.6 torr, p<0.001) that followed the bradycardia. SAD abolished the bradycardia and the hypertension after uterine blood flow reduction. We also injected cyanide (CN) into the fetal inferior vena cava (25-150 μg/kg, n=10) to stimulate the chemoreceptors. CN produced a 35% fall in HR and variable BP changes. CN did not affect HR or aortic pressure in the SAD fetuses, but with carotid denervation alone, bradycardia and hypertension still occurred. Thus, aortic and carotid chemoreceptors are active in utero and are responsible for the HR and blood pressure changes during acute fetal hypoxia. (Supported by NIH grants HL 06285 and HL 24056.)
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