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Does the application of transthoracic electrical discharges cause mitochondrial injuries in atrial cardiac cells of rats?
Does the application of transthoracic electrical discharges cause mitochondrial injuries in atrial cardiac cells of rats?
Transthoracic electrical discharges induce transient mitochondrial injuries (edema and lysis) in atrial cardiac cells of rats that appear to resolve by 7 days.
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Transient mitochondrial injury after transthoracic discharge in rats is hypothesis-generating; leaves open clinical relevance in humans.
BACKGROUND: Cardiomyocytes cytoarchitecture changes caused by transthoracic countershocks have been focused recently. We aimed to evaluate the effects of electrical discharge application in the mitochondria structure in atrial myocardium of rats. METHODS: An electrical cardioverter was adapted to small rodent animals for our research. Electrical discharges were applied to the precordial region of 30 albino rats: (1) control group - animals that remained on resting period and were afterwards sacrificed; (2) electrical discharge group - animals that remained on resting period, followed by ten electrical discharges of 300 mV and sacrificed, and; (3) electrical post-discharge group - animals that remained on a resting period and received ten electrical discharges like the electrical discharge group, but were sacrificed seven days subsequently. We examined liver, adrenal and left atrium tissue fragments of the three groups. RESULTS: It was observed in control and post-discharge groups a normal cellular structure aspect with preserved architecture of cardiomyocytes and continuous sarcoplasmic membrane integrity. On the other hand, cardiac muscle fibers with mitochondrial edema and lysis occurred in the discharge group. Glycogen and adrenal lipids were not depleted in all groups. CONCLUSION: These data suggest that transthoracic electrical discharges induce mitochondrial injuries in atrial cardiac cells of rats.
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Ferreira et al. (2009) studied this question.
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