ABNORMAL INTRACELLULAR CALCIUM HANDLING IN MYOCARDIUM FROM PATIENTS WITH END-STAGE HEART-FAILURE
ABNORMAL INTRACELLULAR CALCIUM HANDLING IN MYOCARDIUM FROM PATIENTS WITH END-STAGE HEART-FAILURE
复制标题
DOI：
10.1161/01.res.61.1.70
复制
发表时间：
1987-07-01
影响因子：
20.1
通讯作者：
MORGAN, JP
中科院分区：
文献类型：
--
作者：
GWATHMEY, JK;COPELAS, L;MORGAN, JP
细胞内钙的释放和重摄取是正常心肌收缩和松弛所必需的。用Aequorin记录终末期心力衰竭患者心肌等长收缩过程中的细胞内钙瞬变。与对照组相比，衰竭心脏肌肉的收缩和钙瞬变明显延长，而钙瞬变表现出两个不同的成分。心脏衰竭的肌肉在舒张期恢复低静息钙水平的能力减弱。这些实验首次从主动收缩的人类心肌中提供了细胞内钙处理异常的直接证据，并可能导致心力衰竭时的收缩和舒张期功能障碍。
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.