Cardiovascular Responses to Hypoxemia in Sinoaortic-Denervated Fetal Sheep

Abstract

Fetal cardiovascular response to acute hypoxemia is characterized by bradycardia, hypertension, and redistribution of cardiac output. The role of aortic and carotid chemoreceptors in mediating these responses was examined in eight sinoaortic-denervated and nine sham-operated fetal lambs. Blood gases, pH, heart rate, arterial pressure, and blood flow distribution were determined before and during hypoxemia. In intact fetuses, heart rate fell from 184 ± 12 to 165 ± 23 beats/min (p < 0.01) but increased from 184 ± 22 to 200 ± 16 beats/min (p < 0.05) in the sinoaortic-denervated fetuses. Intact fetuses showed an early hypertensive response to hypoxemia, whereas the sinoaortic-denervated fetuses developed a delayed, progressive rise in blood pressure. In both groups, fetal cardiac output and umbilical blood flow were maintained; cerebral, myocardial, and adrenal blood flow increased, and pulmonary blood flow decreased. Peripheral blood flow decreased 39% (p < 0.001) in intact fetuses but was maintained in sinoaortic-denervated fetuses. Vascular responses to hypoxia in the brain, heart, adrenal, and lungs are regulated primarily by direct local effects. During hypoxemia, peripheral chemoreceptors mediate bradycardia and peripheral vasoconstriction but do not appear to be crucial for immediate fetal survival. (Pediatr Res 30: 381–385, 1991)