Gwathmey J K, Copelas L, MacKinnon R, Schoen F J, Feldman M D, Grossman W, Morgan J P
Circ Res. 1987 Jul;61(1):70-6. doi: 10.1161/01.res.61.1.70.
Intracellular Ca2+ release and reuptake are essential for contraction and relaxation of normal heart muscle. Intracellular Ca2+ transients were recorded with aequorin during isometric contraction of myocardium from patients with end-stage heart failure. In contrast to controls, contractions and Ca2+ transients of muscles from failing hearts were markedly prolonged, and the Ca2+ transients exhibited 2 distinct components. Muscles from failing hearts showed a diminished capacity to restore low resting Ca2+ levels during diastole. These experiments provide the first direct evidence from actively contracting human myocardium that intracellular Ca2+ handling is abnormal and may cause systolic and diastolic dysfunction in heart failure.
细胞内钙离子的释放和再摄取对于正常心肌的收缩和舒张至关重要。在终末期心力衰竭患者的心肌等长收缩过程中，用发光蛋白记录细胞内钙离子瞬变。与对照组相比，衰竭心脏肌肉的收缩和钙离子瞬变明显延长，并且钙离子瞬变呈现出两个不同的成分。衰竭心脏的肌肉在舒张期恢复低静息钙离子水平的能力减弱。这些实验提供了来自主动收缩的人心肌的首个直接证据，即细胞内钙离子处理异常，可能导致心力衰竭时的收缩和舒张功能障碍。
