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心力衰竭是心肌梗死、心肌炎、高血压、心脏瓣膜病等多种心脏疾病的最终发展结果,其患病率及病死率较高。既往认为,心力衰竭是心室功能的异常,近年来逐渐认识到,心室重构是心力衰竭发生、发展的分子细胞学基础,其能全面影响心室的功能状态及生存预后,是心力衰竭患者患病率和病死率的决定因素。内皮素是心室重构的重要致病因子,可促进心肌细胞和成纤维细胞的病理性增殖,使胶原纤维分泌增加,在心肌间质和血管周围沉积,引起心肌顺应性下降,舒缩功能障碍并通过介导血管紧张素Ⅱ刺激成纤维细胞的有丝分裂,合成Ⅰ型和Ⅲ型胶原,抑制胶原酶活性,促进胶原的合成与分泌,从而促进心室重构。心力衰竭时血浆内皮素水平显著升高,影响心室重构的发生和发展。内皮素受体拮抗剂具有拮抗内皮素的生物效应,抑制内皮素与受体相结合,从而改善心室重构,降低心力衰竭发病率及病死率,改善预后,提示内皮素参与了心室重构的发生、发展。
Heart failure is the final result of many heart diseases such as myocardial infarction, myocarditis, hypertension and valvular heart disease, and its prevalence and mortality are high. Past thought, heart failure is an abnormal ventricular function, in recent years gradually realized that ventricular remodeling is the basis of molecular cytology of the occurrence and development of heart failure, which can fully affect the ventricular function and survival prognosis of patients with heart failure The determinants of rates and fatality rates. Endothelin is an important virulence factor of ventricular remodeling, which can promote the pathological proliferation of cardiomyocytes and fibroblasts, increase the secretion of collagen fibers, deposit in the myocardial interstitium and blood vessels, cause the decrease of myocardial compliance and the systolic and diastolic dysfunction And through the mediation of angiotensin Ⅱ stimulated fibroblast mitosis, synthesis of type I and type III collagen, inhibition of collagenase activity, and promote collagen synthesis and secretion, thereby promoting ventricular remodeling. Heart failure plasma endothelin levels were significantly increased, affecting the occurrence and development of ventricular remodeling. Endothelin receptor antagonists antagonize the biological effects of endothelin, inhibiting the combination of endothelin and receptor to improve ventricular remodeling, reduce the incidence of heart failure and mortality, improve prognosis, suggesting that endothelin is involved in ventricular remodeling Occurrence and development.