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

Citation
T. Kiserud et al., Effect of NO, phenylephrine, and hypoxemia on ductus venosus diameter in fetal sheep, AM J P-HEAR, 279(3), 2000, pp. H1166-H1171
Citations number
30
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
279
Issue
3
Year of publication
2000
Pages
H1166 - H1171
Database
ISI
SICI code
0363-6135(200009)279:3<H1166:EONPAH>2.0.ZU;2-9
Abstract
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.