Abstract
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.
Original language | English (US) |
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Pages (from-to) | 70-76 |
Number of pages | 7 |
Journal | Circulation research |
Volume | 61 |
Issue number | 1 |
DOIs | |
State | Published - 1987 |
Externally published | Yes |
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine