慢性肺心病患者血浆内皮素和凝血、纤溶指标的变化

Relationship Between Endothelin and Blood Coagulation and Fibrinolysis in Pulmonary Heart Disease

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。

Plasma levels of endothelin (ET), von Willebrand factor, anti-thrombin Ⅲ,fibrincgen,fibrin degradation product, tissue type plasminogen activator and plasminogen activator inhibitor were studied in thirty patients with pulmonary heart disease and blood gas analysis was performed in some severe cases. During both exacerbation and remission stages ,the endothelin levels were significantly increased and blood coagulation-fibrinolysis equilibrium was disturbed. ET level was negatively correlated with PaO2(r=-0.561,P<0.01). Hypercoagulability of blood was present in patients with chronic pulmonary heart disease,especially in exacerbation stage. Hypoxia causes the injury of the endothelial cells which is aggravated by the elevated ET level and leads to further disequilibrium between blood coagulation and anticoagulation substances, lowered fibrinolytic activity and marked hypercoagulability status of the blood. Both factors mutually interact and play an important role in the development of complications of pulmonary heart disease.