Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure.

作者：Judith K. Gwathmey, L Copelas, Roderick MacKinnon, F J Schoen, M D Feldman, William Grossman, James P. Morgan · 发表于：Circulation Research · 年份：1987 · DOI：10.1161/01.res.61.1.70 · 被引用次数：926 · 研究领域：Neuroscience and Neural Engineering、bioluminescence and chemiluminescence research、Electrochemical sensors and biosensors

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.