Kiserud T, Ozaki T, Nishina H, Rodeck C, Hanson M A
Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, London WC1E 6HX, United Kingdom.
Am J Physiol Heart Circ Physiol. 2000 Sep;279(3):H1166-71. doi: 10.1152/ajpheart.2000.279.3.H1166.
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 PO(2) (PaO(2)) 24 mmHg] were compared with measurements during infusion of sodium nitroprusside (SNP; 1.3, 2.6, and 6.5 microg. kg(-1). min(-1)) or the alpha(1)-adrenergic agonist phenylephrine (6.5 microg. kg(-1). min(-1)) into the umbilical vein or during hypoxemia (fetal Pa(O(2)) 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.
为了在体内研究静脉导管（DV）入口的调节，我们在氯胺酮 - 地西泮麻醉下，对9只处于0.9妊娠期的子宫内胎羊，测量了血管活性物质和低氧血症对其直径的影响。将导管插入脐静脉和胎儿颈总动脉，并在脐静脉周围放置流量计。将常氧基线条件下（胎儿动脉血氧分压[PaO₂]为24 mmHg）胎儿DV直径的超声测量结果，与脐静脉输注硝普钠（SNP；1.3、2.6和6.5 μg·kg⁻¹·min⁻¹）或α₁ - 肾上腺素能激动剂去氧肾上腺素（6.5 μg·kg⁻¹·min⁻¹）期间，或低氧血症（胎儿PaO₂降至10 mmHg）期间的测量结果进行比较。SNP使DV入口直径增加了23%，但去氧肾上腺素没有影响。低氧血症导致入口直径增加61%，并使整个血管扩张。我们得出结论，DV入口处于张力性收缩状态，因为一氧化氮可使其扩张，但α₁ - 肾上腺素能激动剂不会增强收缩。低氧血症会导致整个DV明显扩张。
