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目的 测定妊高征患者中的凝固 -纤溶因子的变化 ,探讨胎盘局部凝固 -纤溶系统的调节及其在妊高征发病机制中的作用。 方法 用放射免疫法测定重度妊高征及正常孕妇的羊水、母体血浆及胎盘组织中纤溶酶原激活物抑制剂 1型 (PAI- 1)、凝血酶抗凝血酶 复合物 (TAT)及 D双聚体(D- dim er)的含量 ,用人胎盘蜕膜细胞培养系统进行凝血酶负荷试验。 结果 在正常妊娠的 PAI- 1、TAT在羊水中含量分别为 (80 9.2± 79.8) ,(872± 2 14) ng/ ml,明显高于母体血浆的 (140 .9± 38.3) ,(6 .1± 0 .4) ng/ m l,胎盘组织中 PAI- 1含量 ,蜕膜组织 (415 .7± 39) ng/ m g明显高于绒毛组织 (93.9±10 ) ng/ m g。在妊高征患者 ,羊水及胎盘蜕膜组织 PAI- 1分别为 (1474.5± 2 5 4.7) ng/ ml及(116 4± 132 ) ng/ mg蛋白、TAT(132± 2 5 3.1) ng/ m l,D- dimer(132± 2 7.8) ng/ m l显著高于正常妊娠。凝血酶可刺激胎盘蜕膜细胞增加 PAI- 1的产生和分泌 ,两者存在着量效关系。 结论 妊高征中胎盘蜕膜细胞产生和分泌 PAI- 1水平的增加 ,使胎盘凝固 -纤溶系统发生改变 ,即凝固亢进 ,纤溶活性降低。这些改变可能与妊高征发病机制有关。
Objective To determine the changes of coagulation - fibrinolysis factor in patients with pregnancy induced hypertension and to explore the regulation of local coagulation - fibrinolysis system and its role in the pathogenesis of pregnancy induced hypertension. Methods Radioimmunoassay was used to determine the expression of PAI-1, TAT and serum levels of amniotic fluid, maternal plasma and placental tissue in patients with severe PIH and normal pregnant women. D dimer (D-dim er) content, human placental decidual cell culture system for thrombin load test. Results In normal pregnancy, the contents of PAI-1 and TAT in amniotic fluid were (80 9.2 ± 79.8) and (872 ± 2 14) ng / ml, respectively, which were significantly higher than those of maternal plasma (140.9 ± 38.3) and (6) 1 ± 0.4 ng / ml. The content of PAI-1 in placenta tissue was significantly higher than that in villi tissue (93.9 ± 10) ng / mg, (415.7 ± 39) ng / mg. In PIH patients, amniotic fluid and placental decidual tissue PAI-1 were (1474.5 ± 2.54) ng / ml and (116 4 ± 132) ng / mg protein, TAT , D-dimer (132 ± 2 7.8) ng / ml was significantly higher than normal pregnancy. Thrombin can stimulate the placental decidual cells to increase PAI-1 production and secretion, there is a dose-effect relationship between the two. Conclusions The increase of PAI-1 production and secretion in placental decidual cells during pregnancy-induced hypertension leads to the change of coagulation-fibrinolysis system in the placenta, namely, the enhancement of coagulation and the decrease of fibrinolytic activity. These changes may be related to the pathogenesis of PIH.