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Intracellular calcium handling in isolated ventricular myocytes from patients with terminal heart failure
D J Beuckelmann1, M Näbauer, E Erdmann
1Department of Medicine I, University of Munich, FRG.
Insights
Heart failure patients show altered excitation-contraction coupling in ventricular myocytes. Diseased cells exhibit higher resting intracellular calcium and slower calcium decline, impacting contractility.
Area of Science:
- Cardiology
- Cell Physiology
- Biochemistry
Background:
- Investigated excitation-contraction coupling in human ventricular myocytes from heart failure patients.
- Compared myopathic cells (dilated/ischemic cardiomyopathy) with healthy donor cells.
Purpose of the Study:
- To investigate properties of excitation-contraction coupling in terminal heart failure.
- To understand cellular mechanisms underlying altered contractility in heart failure.
Main Methods:
- Isolated human ventricular myocytes from heart failure and control groups.
- Recorded intracellular calcium ([Ca2+]i) transients and calcium currents using fura 2 indicator under voltage clamp.
- Stimulated cells externally and recorded action potentials in current clamp mode.
Main Results:
- No significant difference in unstimulated calcium current densities between myopathic and control cells.
- Diseased myocytes had higher resting intracellular calcium (165 nmol/l vs. 95 nmol/l).
- Peak intracellular calcium transients were lower in myopathic cells (367 nmol/l vs. 746 nmol/l) and declined slower during diastole due to prolonged action potentials and reduced sarcoplasmic reticulum calcium sequestration.
Conclusions:
- Altered intracellular calcium handling contributes to impaired contractility in heart failure.
- Findings may partly explain in vivo contractility alterations in heart failure patients.
Background:
Experiments were performed in human ventricular myocytes to investigate properties of excitation-contraction coupling in patients with terminal heart failure. Myocytes were isolated from left ventricular myocardium of patients with cardiac failure caused by dilated or ischemic cardiomyopathy undergoing transplantation. These results were compared with those obtained from cells of healthy donor hearts that for technical reasons were not suitable for transplantation.
Methods And Results:
[Ca2+]i transients and Ca2+ currents were recorded from isolated cells under voltage clamp perfused internally with the Ca2+ indicator fura 2. In cells that were stimulated externally, the cell-permeant form of the indicator, fura 2-AM, was used. When action potentials were to be recorded, cells were stimulated in current clamp mode. Unstimulated Ca2+ current densities were not significantly different in myopathic and control cells. In diseased myocytes, resting [Ca2+]i levels were 165 +/- 61 nmol/l, compared with 95 +/- 47 nmol/l in normal cells. With 5 mmol/l Na+ in the pipette, peak [Ca2+]i transients were 367 +/- 109 and 746 +/- 249 nmol/l, respectively. The decline of [Ca2+]i during diastole was significantly slower in myopathic cells than in control cells. This was a result of a prolongation of the action potential and of a reduced Ca2+ sequestration by the sarcoplasmic reticulum.
Conclusions:
These results may partly explain the alterations of contractility in vivo in patients with heart failure.
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