Morrow R J, Adamson S L, Bull S B, Ritchie J W
Department of Obstetrics and Gynecology, University of Toronto, Ontario, Canada.
Am J Obstet Gynecol. 1990 Oct;163(4 Pt 1):1313-20. doi: 10.1016/0002-9378(90)90712-g.
The effect of hypoxic acidemia, hyperviscosity, and maternal hypertension on the umbilical arterial velocity waveform was studied in 23 chronically catheterized fetal sheep. Fetal hypoxic acidemia induced by lowering the maternal inspired oxygen concentration (n = 7) caused no change in the ratio of systolic/diastolic blood velocity even when fetal arterial pH was as low as 6.8. Fetal blood hyperviscosity (n = 7) induced by exchange transfusion with packed maternal blood cells increased placental vascular resistance by greater than or equal to 50% but had no significant effect on the systolic/diastolic ratio. Similarly, maternal hypertension induced by intravenous infusion of angiotensin II to the ewe (n = 9) did not affect the systolic/diastolic ratio despite a 50% increase in maternal arterial blood pressure. We conclude that umbilical arterial velocity waveform abnormalities observed in growth-restricted human fetuses are probably not a direct result of fetal hypoxemia or hyperviscosity or maternal hypertension.
在23只长期插管的胎羊中研究了低氧血症、高粘滞血症和母体高血压对脐动脉血流速度波形的影响。通过降低母体吸入氧浓度诱导胎儿低氧血症（n = 7），即使胎儿动脉pH低至6.8，收缩期/舒张期血流速度比值也未发生变化。用母体浓缩血细胞进行换血诱导胎儿血液高粘滞血症（n = 7），使胎盘血管阻力增加≥50%，但对收缩期/舒张期比值无显著影响。同样，给母羊静脉输注血管紧张素II诱导母体高血压（n = 9），尽管母体动脉血压升高50%，但未影响收缩期/舒张期比值。我们得出结论，在生长受限的人类胎儿中观察到的脐动脉血流速度波形异常可能不是胎儿低氧血症、高粘滞血症或母体高血压的直接结果。
