Taylor R N, de Groot C J, Cho Y K, Lim K H
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco 94143, USA.
Semin Reprod Endocrinol. 1998;16(1):17-31. doi: 10.1055/s-2007-1016249.
During the past decade a new hypothesis has been formulated that explains many of the disparate findings associated with the pregnancy syndrome preeclampsia. With an increased awareness of the physiological significance of vascular endothelial cell function, the seemingly unrelated signs of hypertension, proteinuria, edema, and hypercoagulability have converged to provide clinical evidence of a unifying pathophysiological mechanism: systemic, maternal endothelial cell dysfunction. Investigators have attempted to test this hypothesis through two approaches. The first approach involves the identification of in vivo markers of vascular endothelial cell injury in women with clinically evident preeclampsia. The second approach focuses on the ability of circulating factors derived from the serum or plasma of patients afflicted with preeclampsia to perturb endothelial cell function in vitro. In this review we summarize the increasingly compelling evidence that maternal vascular endothelial cells are a critical target for toxic humoral activities that precipitate the multifaceted preeclampsia syndrome.
在过去十年里，一种新的假说被提出，该假说解释了许多与先兆子痫妊娠综合征相关的不同发现。随着对血管内皮细胞功能生理意义的认识不断提高，高血压、蛋白尿、水肿和高凝状态这些看似不相关的症状已趋于一致，为一种统一的病理生理机制提供了临床证据：全身性的母体血管内皮细胞功能障碍。研究人员试图通过两种方法来验证这一假说。第一种方法是识别临床诊断为先兆子痫的女性体内血管内皮细胞损伤的标志物。第二种方法聚焦于先兆子痫患者血清或血浆中循环因子在体外干扰内皮细胞功能的能力。在这篇综述中，我们总结了越来越多令人信服的证据，即母体血管内皮细胞是引发多方面先兆子痫综合征的毒性体液活动的关键靶点。
