妊高征患者纤溶酶原激活物抑制剂1型,凝血酶抗凝血酶Ⅲ复合物及D双聚体的变化

The Changes of Plasminogen Activator Inhibitor Type 1,Thrombin Anti-thrombin Ⅲ comlplex and D-dimer in Patients with Preeclampsia

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 investigated the molecular markers of coagulation fibrinolytic system plasminogen activator inhibitor type 1 (PAI 1), thrombin anti thrombin Ⅲ complex (TAT) and D dimer in amniotic fluid (AF), maternal plasma, as well as the effect of thrombin on PAI 1 production by term decidual cells, to evaluate the regulatory mechanisms of the fibrinolysis system in local placenta Methods Amniotic fluid were obtained by amniocentesis done for genetic indication or during elective cesarean section. Blood samples were collected by venipunture at 17～20 weeks and at term.Placental tissue were homogenized in Tri HCL buffer with Tween 80. The term decidual cells were cultured by the gradient percoll method. PAI 1, D dimer, TAT were measured by ELISA. Results PAI 1 and TAT levels in AF [(809±79), (872 8±214) ng/ml±s respectively] were extremely higher than maternal plasma ( P <0.001) during normal pregnancy at term. A 3～4 fold higher PAI 1 level was found in the homogenates of decidua as compared to that in villi and amnio membrane ( P <0.01). As to preeclampsia, the significantly higher levels of PAI 1, TAT, D dimer (1474.5±254.7),(5 000±253.1), (132±28) ng/ml respectively were found in AF and placental decidua (1164±132 ng/mg protein), as compared to the normals ( P <0.01). PAI 1 production by decidual cells was induced by thrombin in a time dose dependent manner. Conclusions The increased decidual PAI 1 level, resulting in the alternation of the higher coagulation and depressed fibrinolysis in placenta might be involved in the pathogenesis of preeclampsia.