Читать книгу Genetic Disorders and the Fetus - Группа авторов - Страница 145

Placental angiogenesis and vasculogenesis serves to increase both uterine (maternal) and umbilical (fetal) blood flow. This process is dependent on a balance between pro‐ and antiangiogenic factors.¹⁷ Early in pregnancy, EVTs invade and plug the maternal uterine arteries, helping to maintain a low‐oxygen environment needed for trophoblast proliferation.¹⁸ Trophoblast cells (eCTBs) also migrate along the lumina of spiral arterioles, replacing the maternal endothelial lining. This expands the diameter of the maternal vessels and, in combination with gradual disintegration of the spiral artery plugs, results in a dramatic increase in blood flow after 12 weeks gestational age, which is needed to support fetal growth later in pregnancy. In turn, placental vasculature develops, and increases throughout gestation as the needs of the fetus grow.¹⁹ FGR can result from poor spiral artery remodeling or reduced vascular development within the placenta. Furthermore, insufficient remodeling of the maternal spiral arteries can result in a prolonged state of hypoxia and increased reoxygenation stress. This leads to increased syncytiotrophoblast apoptosis and necrosis, causing increased debris circulating in the maternal blood that has been associated with maternal PE.²⁰ In addition to FGR and PE, abnormal spiral artery remodeling has been associated with placental abruption, preterm premature rupture of membranes, and intrauterine fetal death.²¹