Metabolic Changes and Mitochondrial Dysfunction Early Following Transthoracic Countershock in Dogs

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Abstract
TROUTON, T.G., et al.: Metabolic Changes and Mitochondrial Dysfunction Early Following Transthoracic Countershock in Dogs The mechanisms of myocardial injury and necrosis /ollon'ing transfhoracic shocks from a direct current cardiac defibrillator were investigated in adult greyhounds. Myocardial lactate extraction became negative maximally at 1 minute, following two (mean –22%± SEM 23) or five (–193%± 135) shocks and returned to baseline in 6–15 minutes. Myocardial necrosis assessed at 4 hours following the shock period was 0.05 g (± 0.03) after two shocks, 6.69 g (± 1.76) after five shocks and zero in controls. In further experiments, dogs received five or zero (dummy) shocks and mitochondria were isolated from their hearts following excision within 1 minute of receiving the final shock. Maximal oxygen consumption in right ventricular mitochondria was lower than the unshocked controls ivith both giutamate (66.9 ± 9.4 nanoatoms of oxygen/mg per minute, n = 9 vs 86.6 ± 13.6 nanoatoms/mg per minute, n = 7) and succinate (96.2 ± 8.7 nanoatoms/mg per minute, n - 9 vs 119.5 ± 14.4 nanoatoms/mg per minute, n = 7) as substrates. Using electron spin resonance spectroscopy, an increase in a peroxyl-free radical with g = 2.031 was detected in myocardial tissue after two internal shocks (50 joules stored energy, 0.5-minute intervals). We conclude that mitochondria) dysfunction and free-radical generation are likely contributors to cellular injury following multiple countershocks.