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Mitochondrial membrane potentials in ischemic hearts.
Deborah A Berkich1, Guy Salama, Kathryn F LaNoue
1Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA.
Archives of Biochemistry and Biophysics
|December 5, 2003
Summary
The mitochondrial permeability transition plays a role in ischemic cell death. This process is not triggered by calcium influx but is delayed by cyclosporin A.
Area of Science:
- Cardiovascular Physiology
- Mitochondrial Biology
- Ischemic Pathophysiology
Background:
- Global ischemia leads to impaired heart function and cell death.
- Mitochondrial dysfunction is a key factor in ischemic injury.
- The mitochondrial permeability transition (MPT) is implicated in cell death pathways.
Purpose of the Study:
- To investigate the role of mitochondrial electrical potential gradients (Deltapsi(m)) during ischemia-reperfusion.
- To correlate Deltapsi(m) with mechanical performance and high-energy phosphates.
- To determine the role of calcium and the MPT in ischemic cell death.
Main Methods:
- Isolated rat hearts subjected to global ischemia and reperfusion.
- Measurement of in situ Deltapsi(m) using 3H-tetraphenylphosphonium.
- Assessment of cardiac mechanical performance and high-energy phosphates.
Main Results:
- Deltapsi(m) dropped sharply after 35 minutes of ischemia, paralleling mechanical failure.
- Calcium removal from reperfusate did not preserve Deltapsi(m) or high-energy phosphates.
- Cyclosporin A delayed, but did not prevent, the fall in Deltapsi(m).
Conclusions:
- The mitochondrial permeability transition is involved in ischemic cell death.
- MPT is not triggered by plasma membrane calcium influx.
- MPT plays a significant role in the pathophysiology of myocardial ischemia.