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The role of peripheral chemoreceptors in the rapid response of the pulmonary vasculature of the late gestation sheep fetus to changes in PaO2.

The effect of removing the input from the peripheral arterial chemoreceptors on pulmonary vascular responses to changes in PaO2 was examined in late gestation fetal sheep. Blood flow in the left pulmonary artery and driving pressure across the pulmonary vascular bed were monitored in chronically prepared fetal sheep at 126-129 days gestation. Five fetuses had carotid sinus and vagus nerves sectioned bilaterally and four were left intact. In normoxia (PaO2 ca. 23 mmHg) pulmonary vascular resistance was slightly greater and pulmonary blood flow reduced in the denervated group relative to the intact group but these differences were not significant. When made hypoxic (PaO2 ca. 14 mmHg), pulmonary blood flow fell and pulmonary vascular resistance increased in all fetuses. However, in the intact fetuses these changes were significantly more rapid. In all fetuses the vasoconstriction was prolonged after their return to normoxia. When made hyperoxic (PaO2 ca. 27 mmHg), pulmonary blood flow increased by a similar amount in all fetuses. We conclude that in the term fetus the peripheral chemoreceptors play no appreciable role in the maintenance of the high pulmonary vascular resistance in normoxia, or the fall in resistance produced by a rise in PaO2. The chemoreceptors do however initiate the rapid phase of pulmonary vasoconstriction in hypoxia.