LaMarca Babbette, Amaral Lorena M, Harmon Ashlyn C, Cornelius Denise C, Faulkner Jessica L, Cunningham Mark W
Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
Curr Hypertens Rep. 2016 Apr;18(5):38. doi: 10.1007/s11906-016-0633-x.
Preeclampsia is new onset (or worsening of preexisting) hypertension that occurs during pregnancy. It is accompanied by chronic inflammation, intrauterine growth restriction, elevated anti-angiogenic factors, and can occur with or without proteinuria. Although the exact etiology is unknown, it is thought that preeclampsia begins early in gestation with reduced uterine spiral artery remodeling leading to decreased vasculogenesis of the placenta as the pregnancy progresses. Soluble factors, stimulated by the ischemic placenta, shower the maternal vascular endothelium and are thought to cause endothelial dysfunction and to contribute to the development of hypertension during pregnancy. Due to the difficulty in studying such soluble factors in pregnant women, various animal models have been designed. Studies from these models have contributed to a better understanding of how factors released in response to placental ischemia may lead to increased blood pressure and reduced fetal weight during pregnancy. This review will highlight various animal models and the major findings indicating the importance of placental ischemia to lead to the pathophysiology observed in preeclamptic patients.
子痫前期是孕期新发（或原有病情加重）的高血压。它伴有慢性炎症、子宫内生长受限、抗血管生成因子升高，可伴有或不伴有蛋白尿。虽然确切病因尚不清楚，但认为子痫前期在妊娠早期就开始了，随着妊娠进展，子宫螺旋动脉重塑减少，导致胎盘血管生成减少。缺血胎盘刺激产生的可溶性因子作用于母体血管内皮，被认为会导致内皮功能障碍，并促使孕期高血压的发展。由于在孕妇中研究此类可溶性因子存在困难，因此设计了各种动物模型。来自这些模型的研究有助于更好地理解胎盘缺血时释放的因子如何导致孕期血压升高和胎儿体重减轻。本综述将重点介绍各种动物模型以及主要研究结果，这些结果表明胎盘缺血对于导致子痫前期患者所观察到的病理生理学变化具有重要意义。
