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The calcium paradox: a reaffirmation
Insights
Reperfusion of isolated rat hearts with calcium causes irreversible damage, leading to loss of heart activity and release of intracellular enzymes. This damage occurs regardless of constant pressure or flow perfusion methods.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Calcium plays a critical role in cardiac function.
- Sudden changes in calcium levels can significantly impact heart tissue.
Purpose of the Study:
- To investigate the effects of calcium-containing medium perfusion on isolated rat hearts after a calcium-free period.
- To determine the impact on electrical and mechanical activity and intracellular component release.
Main Methods:
- Isolated rat hearts were perfused with calcium-free medium, followed by perfusion with calcium-containing medium.
- Perfusion was conducted under constant perfusion pressure or constant flow rate conditions.
- Release of intracellular components, such as lactate dehydrogenase, was measured.
Main Results:
- Perfusion with calcium-containing medium induced irreversible loss of electrical and mechanical activity.
- Significant release of intracellular components, including lactate dehydrogenase, was observed.
- These effects were consistent under both constant pressure and constant flow perfusion methods.
Conclusions:
- Reintroduction of calcium after a calcium-free period causes irreversible cardiac damage.
- Lactate dehydrogenase release is a marker of this cellular damage.
- Mechanical activity recovery is not necessary for lactate dehydrogenase release, indicating direct calcium toxicity.
Abstract:
Perfusion of isolated rat hearts with a Ca-2+-containing medium, after a Ca2+-free perfusion period, results in an irreversible loss of electrical and mechanical activity of the heart, as well as a large release of intracellular components such as lactate dehydrogenase. These phenomena can be evoked, when hearts are perfused at a constant perfusion pressure or at a constant flow rate. Evidence is provided that recovery of the mechanical activity of the heart is not a requisite for lactate dehydrogenase release.