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Reperfusion-induced calcium gain after ischemia
J S Elz1, S Panagiotopoulos, W G Nayler
1Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
The American Journal of Cardiology
|March 7, 1989
Summary
Reperfusion causes calcium gain in heart cells, but it
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Biochemistry
Background:
- Reperfusion-induced calcium gain is a marker of irreversible injury.
- The causal relationship between calcium gain and irreversible injury is unclear.
Purpose of the Study:
- To investigate the mechanisms and routes of calcium entry during postischemic reperfusion.
- To determine whether calcium gain triggers or results from irreversible injury.
Main Methods:
- Isolated rat hearts subjected to 30 or 60 minutes of ischemia.
- Reperfusion with modified Krebs-Henseleit buffer (inhibiting contractile activity or oxidative phosphorylation).
- Monitoring of calcium gain and ultrastructural changes, including sarcolemmal integrity.
Main Results:
- Calcium gain during reperfusion is complex and can occur without mitochondrial oxidative phosphorylation.
- Interventions affecting contractile state modulate calcium gain.
- Identified at least two routes of calcium entry: contraction-dependent and contraction-independent.
Conclusions:
- Contraction-dependent calcium entry is linked to sarcolemmal discontinuities.
- Cells can gain excess calcium even when mitochondrial uptake is prevented, suggesting other intracellular binding sites.
- Further research is needed to identify non-mitochondrial calcium binding sites during adenosine triphosphate deprivation.