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11:22
Assessment of Calcium Sparks in Intact Skeletal Muscle Fibers
Published on: February 24, 2014
Dyssynchronous Ca(2+) sparks in myocytes from infarcted hearts
S E Litwin1, D Zhang, J H Bridge
1Division of Cardiology, Veterans Affairs Medical Center, University of Utah, Salt Lake City, Utah, USA. sheldon.litwin@hsc.utah.edu
Circulation Research
|November 25, 2000
Summary
Myocardial infarction impairs heart cell calcium handling, causing slower contractions. Beta-adrenergic stimulation can restore normal calcium cycling in these affected heart cells.
Area of Science:
- Cardiology
- Cellular Biology
- Physiology
Background:
- Heart failure is associated with slowed contractions and calcium (Ca2+) transients in myocytes.
- The underlying mechanisms for these abnormalities in failing hearts remain incompletely understood.
Purpose of the Study:
- To investigate the spatial and temporal characteristics of Ca2+ transients in myocytes from hearts with myocardial infarction (MI).
- To determine the impact of MI on Ca2+ handling and the L-type Ca2+ current.
- To assess the effect of beta-adrenergic stimulation on Ca2+ cycling in MI myocytes.
Main Methods:
- Myocardial infarction was induced in rabbits.
- Confocal microscopy was used to record spatially resolved Ca2+ transients in left ventricular myocytes.
- Field stimulation and pharmacological interventions (isoproterenol) were employed.
Main Results:
- MI myocytes exhibited reduced peak Ca2+ transient amplitudes and prolonged time courses compared to controls.
- Ca2+ transients in MI myocytes were characterized by inhomogeneous increases and localized Ca2+ release.
- Peak L-type Ca2+ current density was reduced in MI myocytes, and the gain function was decreased when calculated by the rate of rise.
- Isoproterenol improved Ca2+ release synchronization in MI myocytes.
Conclusions:
- Poorly coordinated Ca2+ spark production in myocytes from infarcted hearts contributes to abnormal Ca2+ transients.
- These abnormalities can be ameliorated by enhancing protein phosphorylation through beta-adrenergic stimulation.
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