Premium
Metabolic Changes and Mitochondrial Dysfunction Early Following Transthoracic Countershock in Dogs
Author(s) -
TROUTON T.G.,
ALLEN J.D.,
YONG L.K.,
ROONEY J.J.,
ADGEY A.A.J.
Publication year - 1989
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1989.tb01869.x
Subject(s) - medicine , shock (circulatory) , cardiology , necrosis , glutamate receptor , energy metabolism , mitochondrion , endocrinology , biochemistry , biology , receptor
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.