To study the regulation of the ductus venosus (DV) inlet in vivo, we measur
ed the effect of vasoactive substances and hypoxemia on its diameter in nin
e fetal sheep in utero at 0.9 gestation under ketamine-diazepam anesthesia.
Catheters were inserted into an umbilical vein and a fetal common carotid
artery, and a flowmeter was placed around the umbilical veins. Ultrasound m
easurements of the diameter of the fetal DV during normoxic baseline condit
ions [fetal arterial PO2 (PaO2) 24 mmHg] were compared with measurements du
ring infusion of sodium nitroprusside (SNP; 1.3, 2.6, and 6.5 mu g.kg(-1).m
in(-1))or the alpha(1)-adrenergic agonist phenylephrine (6.5 mu g.kg(-1).mi
n(-1)) into the umbilical vein or during hypoxemia (fetal Pa-O2 reduced to
10 mmHg). SNP increased the DV inlet diameter by 23%, but phenylephrine had
no effect. Hypoxemia caused a 61% increase of the inlet diameter and a dis
tension of the entire vessel. We conclude that the DV inlet is tonically co
nstricted, because nitric oxide dilates it but an alpha(1)-adrenergic agoni
st does not potentiate constriction. Hypoxemia causes a marked distension o
f the entire DV.