Hubel C A
Magee-Womens Research Institute and the Department of Obstetrics and Gynecology and Reproductive Sciences, University of Pittsburgh, PA 15213, USA. hubelc+@pitt.edu
Proc Soc Exp Biol Med. 1999 Dec;222(3):222-35. doi: 10.1177/153537029922200305.
The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is substantial evidence to suggest that the diverse manifestations of preeclampsia, including altered vascular reactivity, vasospasm, and discrete pathology in many organ systems, are derived from pathologic changes within the maternal vascular endothelium. With the theme of endothelial cell dysfunction emphasized, this review focuses on the role of oxidative stress (an imbalance favoring oxidant over antioxidant forces) in the pathogenesis of preeclampsia. Data are summarized regarding 1) the role of the placenta in preeclampsia; 2) evidence and mechanisms of oxidative stress in the preeclampsia placenta; 3) markers of oxidative stress in the maternal circulation; and 4) the potential role of maternal dyslipidemia in generation of oxidative stress. A recurrent theme is that free radical reactions, promoted by "cross-talk" between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.
妊娠综合征子痫前期的病因和发病机制仍未得到充分了解。有大量证据表明,子痫前期的多种表现,包括血管反应性改变、血管痉挛以及许多器官系统的离散性病理变化,都源于母体血管内皮的病理改变。以强调内皮细胞功能障碍为主题,本综述重点关注氧化应激(氧化剂与抗氧化剂力量失衡)在子痫前期发病机制中的作用。总结了以下方面的数据:1)胎盘在子痫前期中的作用;2)子痫前期胎盘中氧化应激的证据和机制;3)母体循环中氧化应激的标志物;4)母体血脂异常在氧化应激产生中的潜在作用。一个反复出现的主题是,患病胎盘与母体血脂异常之间的“串扰”所促进的自由基反应,促成了一个恶性循环,使得因果关系难以区分,但可能促进了子痫前期的进展。