Su Emily J
Department of Obstetrics and Gynecology, Divisions of Maternal-Fetal Medicine and Basic Reproductive Science, University of Colorado Denver School of Medicine, Aurora, CO.
Am J Obstet Gynecol. 2015 Oct;213(4 Suppl):S123-30. doi: 10.1016/j.ajog.2015.06.038.
Growth-restricted fetuses with absent or reversed end-diastolic velocities in the umbilical artery are at substantially increased risk for adverse perinatal and long-term outcome, even in comparison to growth-restricted fetuses with preserved end-diastolic velocities. Translational studies show that this Doppler velocimetry correlates with fetoplacental blood flow, with absent or reversed end-diastolic velocities signifying abnormally elevated resistance within the placental vasculature. The fetoplacental vasculature is unique in that it is not subject to autonomic regulation, unlike other vascular beds. Instead, humoral mediators, many of which are synthesized by local endothelial cells, regulate placental vascular resistance. Existing data demonstrate that in growth-restricted pregnancies complicated by absent or reversed umbilical artery end-diastolic velocities, an imbalance in production of these vasoactive substances occurs, favoring vasoconstriction. Morphologically, placentas from these pregnancies also demonstrate impaired angiogenesis, whereby vessels within the terminal villi are sparsely branched, abnormally thin, and elongated. This structural deviation from normal placental angiogenesis restricts blood flow and further contributes to elevated fetoplacental vascular resistance. Although considerable work has been done in the field of fetoplacental vascular development and function, much remains unknown about the mechanisms underlying impaired development and function of the human fetoplacental vasculature, especially in the context of severe fetal growth restriction with absent or reversed umbilical artery end-diastolic velocities. Fetoplacental endothelial cells are key regulators of angiogenesis and vasomotor tone. A thorough understanding of their role in placental vascular biology carries the significant potential of discovering clinically relevant and innovative approaches to prevention and treatment of fetal growth restriction with compromised umbilical artery end-diastolic velocities.
脐动脉舒张末期血流速度消失或倒置的生长受限胎儿，其围产期不良结局及远期不良结局的风险大幅增加，即便与舒张末期血流速度正常的生长受限胎儿相比也是如此。转化研究表明，这种多普勒测速法与胎儿-胎盘血流相关，舒张末期血流速度消失或倒置表明胎盘血管系统内阻力异常升高。胎儿-胎盘血管系统的独特之处在于，与其他血管床不同，它不受自主神经调节。相反，体液介质（其中许多由局部内皮细胞合成）调节胎盘血管阻力。现有数据表明，在伴有脐动脉舒张末期血流速度消失或倒置的生长受限妊娠中，这些血管活性物质的产生会出现失衡，从而有利于血管收缩。从形态学上看，这些妊娠的胎盘还表现出血管生成受损，即终末绒毛内的血管分支稀疏、异常纤细且拉长。这种与正常胎盘血管生成的结构偏差会限制血流，并进一步导致胎儿-胎盘血管阻力升高。尽管在胎儿-胎盘血管发育和功能领域已经开展了大量工作，但对于人类胎儿-胎盘血管系统发育和功能受损的潜在机制，尤其是在伴有脐动脉舒张末期血流速度消失或倒置的严重胎儿生长受限的情况下，仍有许多未知之处。胎儿-胎盘内皮细胞是血管生成和血管舒缩张力的关键调节因子。深入了解它们在胎盘血管生物学中的作用，极有可能发现预防和治疗伴有脐动脉舒张末期血流速度受损的胎儿生长受限的临床相关创新方法。
