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Metabolic changes and mitochondrial dysfunction early following transthoracic countershock in dogs
T G Trouton1, J D Allen, L K Yong
1Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland.
Pacing and Clinical Electrophysiology : PACE
|November 1, 1989
Summary
Multiple defibrillator shocks can cause myocardial injury by impairing mitochondrial function and generating free radicals. This study in greyhounds reveals significant cellular damage and reduced oxygen consumption after repeated transthoracic shocks.
Area of Science:
- Cardiology
- Cellular Biology
- Biochemistry
Background:
- Transthoracic shocks from direct current (DC) cardiac defibrillators are used to treat cardiac arrhythmias.
- The potential for myocardial injury and necrosis following defibrillation is a significant clinical concern.
Purpose of the Study:
- To investigate the mechanisms of myocardial injury and necrosis induced by transthoracic shocks in a canine model.
- To assess the impact of multiple defibrillator shocks on myocardial metabolism and mitochondrial function.
Main Methods:
- Adult greyhounds were subjected to two or five transthoracic DC shocks.
- Myocardial lactate extraction and necrosis were measured at specific time points post-shock.
- Mitochondria were isolated from myocardial tissue within 1 minute of shock delivery for functional assessment (oxygen consumption).
- Electron spin resonance spectroscopy was used to detect free radical generation.
Main Results:
- Myocardial lactate extraction became significantly negative after shocks, indicating anaerobic metabolism.
- Myocardial necrosis increased substantially with five shocks compared to two shocks and controls.
- Maximal oxygen consumption in isolated right ventricular mitochondria was reduced after five shocks.
- A peroxyl-free radical increase was detected in myocardial tissue following two shocks.
Conclusions:
- Mitochondrial dysfunction is a likely mechanism contributing to myocardial injury after defibrillation.
- Free radical generation is implicated in the cellular damage observed following multiple countershocks.
- These findings highlight the cellular consequences of defibrillator use and suggest potential targets for cytoprotection.