Role of catecholamines in mediating fetal blood volume decrease during acute hypoxia.

Abstract

Hypoxia was induced in chronically catheterized sheep fetuses at 133 days gestation (term = 145-150 days) by lowering the O2 content of air inspired by the ewe while supplementing with 1-3% CO2. Control fetal arterial oxygen tension (PO2) averaged 22.5 +/- 0.4 (SE) mmHg. During 30 min of mild hypoxia (PO2 decrease less than 6 mmHg) in normal fetuses, fetoplacental blood volume decreased by 4.7 +/- 0.4% and fetal PO2 by 4.3 +/- 0.7 mmHg. In fetuses with alpha- plus beta-receptor blockade, no change in blood volume occurred during mild hypoxia even though PO2 decreased by 3.4 +/- 0.5 mmHg. During severe hypoxia (PO2 decrease greater than or equal to 6 mmHg), fetal blood volume decreased by 9.2 +/- 1.4% and PO2 by 10.4 +/- 0.4 mmHg in normal fetuses. After adrenergic receptor blockade, blood volume decreased by 7.6 +/- 2.5% when PO2 decreased by 8.0 +/- 0.8 mmHg. Fetal arterial and venous pressure were unchanged during mild hypoxia. Vascular pressures increased significantly during severe hypoxia in normal and blocked fetuses, but these were significantly delayed following adrenergic blockade. Thus, although the catecholamines appear to mediate the decrease in fetal blood volume during mild hypoxia, they appear to have little effect on the blood volume decrease that occurs during severe hypoxia. In addition, the changes in blood volume are not directly correlated with the changes in arterial and venous pressures.