舒张功能不全性心力衰竭分子机制的研究进展  

Molecular Mechanism of Diastolic Heart Failure

作　　者：杨静[1] 陈丽[1] 

机构地区：[1]川北医学院附属医院心内科,四川南充637000

出　　处：《心血管病学进展》2010年第6期916-918,共3页Advances in Cardiovascular Diseases

摘　　要：舒张功能不全性心力衰竭是一种以心力衰竭的症状和体征,正常的射血分数和异常的舒张功能为特征的病理生理综合征。在分子水平上,舒张功能受到心肌肌质网钙泵、钠钙交换体、细胞外基质以及它们的调节蛋白的活动等因素的影响。因此,任何影响上述代谢的因素都可能影响心肌的舒张,并最终发展为舒张功能不全性心力衰竭。现主要阐述近年来舒张功能不全性心力衰竭分子机制的研究进展。Diastolic heart failure is a physiopathologic syndrome,which is characterized by the symptoms and signs of heart failure,a preserved ejection fraction,and abnormal diastolic function.At the molecular level the diastolic function is affected by the activities of the sarcoplasmic reticulum Ca2＋ ATPase,Na＋/Ca2＋ exchanger,extracellular matrix and their regulated proteins.Thus,anything which affects their activities could play a role in the development of diastolic heart failure.This article discusses the molecular mechanism of diastolic heart failure.

关 键 词：心力衰竭 舒张功能不全 分子机制 

分 类 号：R541.61[医药卫生—心血管疾病]