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[妊娠高血压综合征发病机制中的血浆激肽生成与纤维蛋白溶解]

[Plasma kininogenesis and fibrinolysis in the pathogenesis of EPH gestosis].

作者信息

Czokało M, Jaworski S, Buluk K, Rudzinski A

机构信息

Institut für allgemeine und experimentelle Pathologie der Medizinischen Akademie, Bialystok.

出版信息

Zentralbl Gynakol. 1988;110(21):1345-53.

PMID:3213308
Abstract

The coexistence of arterial hypertension and disturbances of haemostasis in pregnant women with EPH-gestosis allow to expect a role of fibrinolysis and kinin-forming systems in pathomechanism of this syndrome. For these reasons blood plasma of 34 patients with EPH-gestosis, 23 patients with normal pregnancy and 19 nonpregnant women was investigated. All pregnant women were in third trimester of pregnancy. The following parameters were investigated: kinin-forming system compounds (kininogens and prokininogenases - biological methods), fibrinolytic activity (plasma euglobulin fibrinolysis time), total plasma protein and fibrinogen concentration, protease inhibitors - antithrombin III, C1-esterase inhibitor, alpha 2-antiplasmin, alpha 1-protease inhibitor and alpha 2-macroglobulin (by electroimmunodiffusion). Furthermore hematocrit was measured. In pregnant women with EPH-gestosis significant increase of high molecular weight kininogen concentration was found (p less than 0.02), decreased fibrinolytic activity (p less than 0.01) and (except alpha 2-antiplasmin) decreased concentration of protease inhibitors (p less than 0.005 - p less than 0.01) were observed. Further statistical analysis demonstrated positive correlation between the concentrations of kininogens and prokallikrein-prokininogenases and between low molecular weight kininogen and plasma euglobulin fibrinolysis time. On the other hand negative correlation between concentrations of those proenzymes and severity of gestosis was observed. The above described phenomena indicate on significance of disturbances of proteolytic enzyme activation in pathogenesis of EPH-gestosis.

摘要

妊娠高血压综合征(EPH-妊娠中毒症)孕妇中动脉高血压与止血功能障碍并存,提示纤维蛋白溶解和激肽形成系统在该综合征发病机制中发挥作用。基于这些原因,对34例EPH-妊娠中毒症患者、23例正常妊娠孕妇及19例未孕女性的血浆进行了研究。所有孕妇均处于妊娠晚期。研究了以下参数:激肽形成系统化合物(激肽原和前激肽原酶——生物学方法)、纤维蛋白溶解活性(血浆优球蛋白溶解时间)、血浆总蛋白和纤维蛋白原浓度、蛋白酶抑制剂——抗凝血酶III、C1酯酶抑制剂、α2抗纤溶酶、α1蛋白酶抑制剂和α2巨球蛋白(通过电免疫扩散法)。此外,还测量了血细胞比容。在EPH-妊娠中毒症孕妇中,发现高分子量激肽原浓度显著升高(p<0.02),纤维蛋白溶解活性降低(p<0.01),且(除α2抗纤溶酶外)蛋白酶抑制剂浓度降低(p<0.005 - p<0.01)。进一步的统计分析表明,激肽原与前激肽释放酶-前激肽原酶浓度之间以及低分子量激肽原与血浆优球蛋白溶解时间之间呈正相关。另一方面,观察到这些酶原浓度与妊娠中毒症严重程度之间呈负相关。上述现象表明蛋白水解酶激活紊乱在EPH-妊娠中毒症发病机制中具有重要意义。

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