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Cardiac reperfusion damage prevented by a nitroxide free radical
D Gelvan1, P Saltman, S R Powell
1Department of Biology, University of California, San Diego, La Jolla 92093.
Summary
This study shows that oxygen-derived free radicals cause reperfusion injury. The stable nitroxide radical TEMPO (2,2,6,6-Tetramethylpiperidine-N-oxyl) significantly reduced reperfusion arrhythmia and cell damage in isolated rat hearts.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Ischemia/reperfusion (I/R) injury is a significant clinical problem.
- Oxygen-derived free radicals are implicated in I/R injury.
- Limited therapeutic options exist to mitigate I/R damage.
Purpose of the Study:
- To investigate the role of oxygen-derived free radicals in I/R injury.
- To evaluate the protective effects of TEMPO against I/R damage in an isolated rat heart model.
Main Methods:
- Regional ischemia was induced in isolated rat hearts.
- Hearts were treated with varying concentrations of TEMPO.
- Reperfusion arrhythmia, lactate dehydrogenase release, and hydroxyl radical formation were measured.
Main Results:
- TEMPO significantly reduced the duration of ventricular fibrillation and tachycardia during reperfusion.
- TEMPO repressed postischemic release of lactate dehydrogenase and hydroxyl radical formation.
- TEMPO's protective effects were observed when administered at the end of ischemia, but not during reperfusion.
Conclusions:
- Reperfusion arrhythmia and cell damage are directly linked to oxidative stress during the initial minute of reperfusion.
- TEMPO protects against I/R injury by preventing hydroxyl radical formation.
- TEMPO's beneficial effects are independent of heart rate reduction or direct anti-arrhythmic action.