卡托普利影响冠心病患者内源性纤溶系统的临床意义及机制

CLINICAL SIGNIFICANCE AND MECHANISM OF CAPTOPRIL EFFECT ON ENDOGENOUS FIBRINOLYTIC SYSTEM IN PATIENTS WITH CORONARY HEART DISEASES

为探讨卡托普利（ｃａｐｔｏｐｒｉｌ）影响冠心病（ＣＨＤ）患者内源性纤溶系统活性的临床意义及机制，选择４５例患者，随机分为治疗组（２３例）及安慰剂对照组（２２例），经处理治疗前血浆各指标参数及治疗后纤维蛋白原、血栓素Ｂ２水平，无统计学意义（Ｐ＞０．０５）；４周后，治疗组血浆血管紧张素Ⅱ（ＡｎｇⅡ）、组织型纤溶酶原激活剂（ｔＰＡ）及其抑制物（ＰＡＩ）活性均显著低于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而６－ｋｅｔｏ－ＰＧＦ１α、ｔＰＡ活性、ｔＰＡ比活性、活性型ｔＰＡ及纤溶活力水平则显著高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）。结论：卡托普利可通过降低血浆ＡｎｇⅡ水平，促进ＣＨＤ患者受损血管内皮细胞修复，减少血管内皮细胞ＰＡＩ的合成与分泌，提高其内源性纤溶系统活性。

In order to discuss the clinical significance and mechanism of captopril effect on endogenous fibrinolytic system activity in patients with coronary heart diseases (CHD), 45 patients were randomly divided into captopril group( n =23),and placebo control group( n =22). Before and after 4 weeks of treatment, the plasma levels of the related indices were assayed in all patients of the two groups.Comparisons of various indices before the therapy, between the two groups were statistically insignificant ( P >0 05). After 4 weeks of therapy,plasma levels of angiotensin Ⅱ, tissue type plasminogen activator(tPA) content and plasminogen activation inhibitor(PA1) activity in the captopril group were significantly lower than those in the control( P <0 05 or 0 01), and 6 keto prostaglandin F 1α ,tPA activity, tPA vs PAI activity, active type tPA and fibrinolytic activity in the captopril group were much higher than those in the control( P <0 05 or 0 01). Plasma levels of fibrinogen (Fg) and thromboxane B 2(TXB 2) were statistically insignificant between the two groups ( P >0 05). It is concluded that captopril can improve the repairment of the damaged endothelial cells, reduce the synthesis and secretion of PAI derived endothelial cells,and increase the activity of endogenous fibrinolysis.