Hemodynamic effects of alpha-adrenergic blockade during hypoxia in fetal sheep.

During hypoxemia there is a redistribution of cardiac output in the sheep fetus associated with increased vascular resistance in some fetal organs. The role of the alpha-adrenergic blocking drug to eight chronically instrumented hypoxemic sheep fetuses. We measured arterial blood pressure and heart rate, determined cardiac output and organ blood flows by means of radionuclide-labeled microspheres, and calculated vascular resistances in fetuses before and during hypoxia, and after injection of phenoxybenzamine 15 mg into the inferior vena cava of the hypoxemic fetus. Hypoxemia resulted in an increased vascular resistance in certain vascular beds. Alpha-adrenergic blockade during hypoxia abolished the increase in vascular resistance of the fetal body and caused an increase in the blood flow to some tissues which had a hypoxia-induced vasoconstriction. After alpha-adrenergic blockade during hypoxia, mean arterial blood pressure decreased from 48 +/- 6 to 42 +/- 6 mm Hg (p less than 0.05) and heart rate increased from 128 +/- 19 to 235 +/- 51 beats per minute (p less than 0.001). Cardiac output increased 23% and blood flow to the brain was maintained. We conclude that the alpha-adrenergic system is important in maintaining the redistribution of cardiac output that occurs in hypoxic fetal sheep.