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Am J Physiol Heart Circ Physiol 279: H1166-H1171, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1166-H1171, September 2000

Effect of NO, phenylephrine, and hypoxemia on ductus venosus diameter in fetal sheep

Torvid Kiserud, Takashi Ozaki, Hidenori Nishina, Charles Rodeck, and Mark A. Hanson

Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, London WC1E 6HX, United Kingdom

To study the regulation of the ductus venosus (DV) inlet in vivo, we measured the effect of vasoactive substances and hypoxemia on its diameter in nine 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 measurements of the diameter of the fetal DV during normoxic baseline conditions [fetal arterial PO2 (PaO2) 24 mmHg] were compared with measurements during infusion of sodium nitroprusside (SNP; 1.3, 2.6, and 6.5 µg · kg-1 · min-1) or the alpha 1-adrenergic agonist phenylephrine (6.5 µg · kg-1 · min-1) into the umbilical vein or during hypoxemia (fetal PaO2 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 distension of the entire vessel. We conclude that the DV inlet is tonically constricted, because nitric oxide dilates it but an alpha 1-adrenergic agonist does not potentiate constriction. Hypoxemia causes a marked distension of the entire DV.

circulation; hypoxia; nitroprusside; vein


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