Pathophysiology of placentation abnormalities in pregnancy-induced hypertension.
Pathophysiology of placentation abnormalities in pregnancy-induced hypertension.
复制标题
妊娠诱导的高血压中胎盘异常的病理生理。
DOI：
10.2147/vhrm.s4009
复制
发表时间：
2008
影响因子：
2.9
通讯作者：
Fukamizu A
中科院分区：
文献类型：
--
作者：
Furuya M;Ishida J;Aoki I;Fukamizu A
在胚胎发生和发育过程中，胎儿通过胎盘微循环从母体获得氧气和营养。胎盘是一个独特的器官，其本身发育和分化，并在整个妊娠过程中组织胎儿生长和母体状况。妊娠期的几种危及生命的疾病，如妊娠高血压综合征（PIH）和子痫，与胎盘功能障碍密切相关。遗传易感性和不良胎盘已经深入研究，以了解妊高征的病理生理。目前认为，“胎盘形成不良假说”，即绒毛外滋养层细胞不能充分侵入胎盘床，部分解释了母体易患这种疾病的原因。累积的研究表明，胎儿胎盘部位的缺氧微环境，子宫胎盘血流的剪切力，以及异常分泌的促炎物质进入母体循环协同促进妊高征的进展。例如，可溶性形式的血管内皮生长因子受体-1（sVEGFR-1）和可溶性形式的CD 105在妊高征母亲的循环中升高。然而，它仍然是知之甚少的病理事件，胎盘在妊娠的后半期，随着母体系统性疾病的恶化。为了更好地了解妊高征和有效的治疗方法，重要的是要澄清妊高征相关的胎盘病变的病理过程。本文就目前对胎盘发育和妊高征胎盘病理生理的认识作一综述。此外，血管活性信号在妊高征和啮齿动物妊高征模型的最新研究结果进行了讨论。
During embryogenesis and development, the fetus obtains oxygen and nutrients from the mother through placental microcirculation. The placenta is a distinctive organ that develops and differentiates per se, and that organizes fetal growth and maternal condition in the entire course of gestation. Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction. Genetic susceptibilities and poor placentation have been investigated intensively to understand the pathophysiology of PIH. It is currently thought that “poor placentation hypothesis”, in which extravillous trophoblasts fail to invade sufficiently the placental bed, explains in part maternal predisposition to this disease. Cumulative studies have suggested that hypoxic micromilieu of fetoplacental site, shear stress of uteroplacental blood flow, and aberrantly secreted proinflammatory substances into maternal circulation synergistically contribute to the progression of PIH. For example, soluble form of vascular endothelial growth factor receptor-1 (sVEGFR-1) and soluble form of CD105 are elevated in circulation of PIH mothers. However, it remains to be poorly understood the pathological events in the placenta during the last half of gestation as maternal systemic disorders get worse. For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta. In this review, current understanding of placental development and the pathophysiology of PIH placenta are summarized. In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.