【摘 要】
：
充血性心力衰竭(CHF)的病理生理机制十分复杂,临床尚缺乏有效的防治方法。血浆内皮素(ET)1水平升高,可通过内皮素受体介导的一系列信号转导途径,导致血管收缩、心肌细胞肥大
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充血性心力衰竭(CHF)的病理生理机制十分复杂,临床尚缺乏有效的防治方法。血浆内皮素(ET)1水平升高,可通过内皮素受体介导的一系列信号转导途径,导致血管收缩、心肌细胞肥大、心室重构,在CHF的发生发展中发挥重要的作用。已有大量关于选择性ET-A受体拮抗剂及非选择性ET受体拮抗剂在治疗CHF方面的动物实验和临床试验结果,为治疗CHF开辟新思路。
The pathophysiological mechanism of congestive heart failure (CHF) is very complicated, and there is no effective prevention and treatment method in clinic. Elevated levels of endothelin (ET) 1 may play an important role in the development and progression of CHF through a series of signal transduction pathways mediated by endothelin receptor, leading to vasoconstriction, cardiomyocyte hypertrophy and ventricular remodeling. There are a large number of animal experiments and clinical trials on selective ET-A receptor antagonists and non-selective ET receptor antagonists in the treatment of CHF, which opens up new ideas for the treatment of CHF.
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