Effects of acute hypercapnia on maternal and fetal vasopressin and catecholamine release

Although fetal asphyxia, i.e. hypoxemia, acidosis, and hypercapnia, increases plasma arginine vasopressin (AVP) >40-fold, hypoxemia and metabolic acidosis occurring independently cause only 5-fold and 2-fold increases, respectively. To determine the effects of hypercapnia on AVP release, we examined the effects of acute hypercapnia on AVP secretion in six pregnant sheep and their fetuses at 135 ± 4 d (x ± SD), exposing the ewe successively to room air, 30% O₂, 30% O₂ plus 10% CO₂, 30% O₂, and room air, and monitoring uterine blood flow, as well as maternal and fetal mean arterial pressure, heart rate, arterial blood gases, and plasma AVP and catecholamines. Oxygen exposure had no effect on the ewe or fetus. During O₂ plus CO₂ exposure, the ewes and fetuses developed hypercapnia in the absence of hypoxia, arterial CO₂ tension increasing to 8.38 ± 0.87 kPa (62.9 ± 6.5 mm Hg) and 10.0 ± 0.61 kPa (75.2 ± 4.6 mm Hg) (p < 0.001), respectively, at 30 min of exposure. Although fetal heart rate and mean arterial pressure were unchanged, maternal values rose 61 and 30% (p < 0.001), respectively. At 30 min of O₂ + CO₂ exposure, maternal norepinephrine increased from 2.23 ± 0.74 to 8.52 ± 3.97 nmol/L (p = 0.15) and fetal epinephrine increased from 0.27 ± 0.10 to 2.271 ± 0.90 nmol/L (p = 0.01); plasma AVP was not significantly increased in the ewe or fetus, although levels rose from ~45 to 127 ± 48 and 137 ± 64 pmol/L (p = 0.10), respectively. Hypercapnia alone is not a major determinant of AVP secretion in the mother or fetus; thus, the marked rise in fetal AVP secretion observed during asphyxial insults may reflect interaction between the effects of hypercapnia and hypoxemia.