Sheppard B L, Bonnar J
University Department of Obstetrics and Gynaecology, Trinity College Centre for Health Sciences, St. James's Hospital and Coombe Women's Hospital Dublin, Ireland.
Semin Thromb Hemost. 1999;25(5):443-6. doi: 10.1055/s-2007-994947.
During pregnancy, extensive hemostatic changes occur in the uteroplacental circulation. Invading endovascular trophoblast cells induce physiological adaptations of uterine spiral arteries, required to accommodate the increased maternal blood flow to the intervillous space of the placenta as pregnancy advances. Much of the vascular endothelium and the underlying medial smooth muscle is replaced by trophoblasts, and fibrin or fibrinoid forms a major morphological feature of the arterial walls. Compared with endothelial cells, the trophoblast lining decidual spiral arteries have a reduced capacity to lyse fibrin, and recent studies have shown this to be caused by high levels of plasminogen activator inhibitors (PAI-1 and PAI-2). In pregnancies complicated by intrauterine fetal growth retardation (IUGR), with or without superimposed preeclampsia, a restricted physiological adaptation of uteroplacental spiral arteries is coupled with vascular lesions containing increased fibrin deposition. Significantly higher levels of PAI-1 are found in blood from the uterine vein at delivery and in tissue extracts of the placenta in these pregnancies than are found in normal pregnancy. Recent tissue culture studies have provided new information on the role of trophoblast cells in maintaining hemostatic control in the uteroplacental circulation in pregnancy. Cytotrophoblast cells isolated from the placenta and placental bed from IUGR pregnancies express significantly higher levels of PAI-1, coupled with a significant decrease in plasminogen activator activity, compared with trophoblast cells from normal pregnancy maintained in culture. This localized increased production of PAI-1 may play an important part in restricting endovascular trophoblast invasion in early pregnancy and increasing fibrin deposition and reducing uteroplacental blood flow in pregnancies complicated by IUGR.
在怀孕期间，子宫胎盘循环会发生广泛的止血变化。侵入血管内的滋养层细胞会诱导子宫螺旋动脉发生生理适应性改变，随着孕期进展，这是为了适应母体向胎盘绒毛间隙增加的血流量所必需的。大部分血管内皮及下方的中层平滑肌被滋养层细胞取代，纤维蛋白或类纤维蛋白形成动脉壁的主要形态学特征。与内皮细胞相比，蜕膜螺旋动脉的滋养层衬里溶解纤维蛋白的能力降低，最近的研究表明这是由高水平的纤溶酶原激活物抑制剂（PAI - 1和PAI - 2）所致。在合并宫内胎儿生长受限（IUGR）的妊娠中，无论有无叠加先兆子痫，子宫胎盘螺旋动脉的生理性适应受限，同时伴有纤维蛋白沉积增加的血管病变。在这些妊娠中，分娩时子宫静脉血以及胎盘组织提取物中PAI - 1的水平显著高于正常妊娠。最近的组织培养研究为滋养层细胞在维持孕期子宫胎盘循环止血控制中的作用提供了新信息。与培养的正常妊娠滋养层细胞相比，从IUGR妊娠的胎盘和胎盘床分离的细胞滋养层细胞表达的PAI - 1水平显著更高，同时纤溶酶原激活物活性显著降低。PAI - 1这种局部产生增加可能在限制妊娠早期血管内滋养层侵入以及增加IUGR妊娠中的纤维蛋白沉积和减少子宫胎盘血流量方面起重要作用。
