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观察３０例肺心病患者血浆内皮素（ＥＴ）、ｖｏｎＷｉｌｌｅｂｒａｎｄ因子、抗凝血酶Ⅲ、纤维原白原（Ｆｇ）、纤维蛋白降解产物（ＦＤＰ）和组织型溶酶原激活物（ＴＰＡ）及其抑制物（ＰＡＩ）。并对部分重症病人进行动脉血气分析。肺心病急性加重期和缓解期，血浆ＥＴ水平明显增高，机体凝血—纤溶功能紊乱。部分重症病人ＥＴ与ＰａＯ２呈负相关（ｒ＝—０．５６１，Ｐ＜０．０１）。提示慢性肺心病患者血液呈高凝状态，加重期明显。低氧是血管内皮细胞损伤的病理基础。ＥＴ水平的增高加重了血管内皮细胞损伤，后者又促使抗凝物、促凝物调节进一步失衡和纤溶活性降低，加重血液的高凝状态。两者互为因果，相互作用，相互影响，在肺心病并发症的发病机理中有重要意义。
The plasma endothelin (ET), von Willebrand factor, antithrombin Ⅲ, fibrinogen (Fg), fibrin degradation product (FDP) and tissue plasminogen activator (TPA) Inhibitor (PAI). And some patients with severe arterial blood gas analysis. Cor Pulmonale acute exacerbation and remission, plasma ET levels were significantly increased, the body coagulation - fibrinolysis disorders. In some critically ill patients, ET was negatively correlated with PaO2 (r = -0.561, P <0.01). Prompted hypercoagulability in patients with chronic pulmonary heart disease, exacerbation of significant. Hypoxia is the pathological basis of vascular endothelial cell injury. Increased ET levels exacerbate vascular endothelial cell damage, which in turn promote the further adjustment of the anticoagulant, coagulant imbalance and fibrinolytic activity, aggravating the blood hypercoagulable state. Both causality, interaction and mutual influence, in the pathogenesis of pulmonary heart disease complications are of great significance.