Figueredo V M, Camacho S A
University of California, San Francisco.
Curr Opin Cardiol. 1994 May;9(3):272-9. doi: 10.1097/00001573-199405000-00003.
The cellular pathophysiology of myocardial dysfunction in heart failure is multifactorial. Studies of animal models and myocardium from patients with heart failure have demonstrated abnormalities of cytosolic calcium handling, myofilament calcium sensitivity, and myocyte energetics. Many of these metabolic abnormalities have been shown to be the result of alterations in the activity or number of myocyte enzymes and transport channels that are important in excitation-contraction coupling. Several innovative techniques for measuring intracellular calcium and energy metabolites and recent advances in cell biology have helped to further our understanding of the cellular pathophysiology of heart failure. Abnormalities at several levels of the excitation-contraction coupling mechanism have been shown to be responsible for both systolic and diastolic dysfunction in the failing heart.
心力衰竭中心肌功能障碍的细胞病理生理学是多因素的。对动物模型和心力衰竭患者心肌的研究表明，细胞溶质钙处理、肌丝钙敏感性和心肌细胞能量代谢存在异常。其中许多代谢异常已被证明是心肌细胞酶和转运通道的活性或数量改变的结果，这些酶和通道在兴奋-收缩偶联中起重要作用。几种测量细胞内钙和能量代谢物的创新技术以及细胞生物学的最新进展有助于加深我们对心力衰竭细胞病理生理学的理解。已证明兴奋-收缩偶联机制多个水平的异常是衰竭心脏收缩和舒张功能障碍的原因。
