Abstract
BackgroundAmiodarone chlorhydrate is a diiodated benzofuran derivative used to treat a variety of cardiac rhythm abnormalities. The use of amiodarone is associated with ultrastructural changes affecting body tissues, but its effect on the ultrastructure of the heart has not yet been fully elucidated.MethodsThe aim of this study is to test the adverse effects of amiodarone administration on cardiomyocytes and to study the possible protective role of vitamin E co-administration. A total of 18 adult male albino rats were used in this study. The rats were divided randomly into three groups of 6 rats each as follows: group I was considered the control group and was given vegetable oil; group II received 54 mg/kg of oral amiodarone; and group III received a single dose of combined vitamin E (50 mg/kg) and amiodarone (54 mg/kg). After 2 weeks, the rats were sacrificed, and the atrial tissues were harvested and processed for electron microscopic study.ResultsAdministration of amiodarone alone modified the atrial architecture, which was demonstrated by the following: mitochondrial enlargement and cristae lysis; marked heterogeneity of myofibril patterns with partial necrosis and disintegration of myofilaments; and irregularities of the sarcomere and less concentration of atrionatriuretic factor (ANF) granules, which localised in closed proximity to the nucleus with disrupted chromatin contents. Concomitant administration of vitamin E with amiodarone showed a considerable preservation of the atrial architecture.ConclusionsOral administration of amiodarone in rats resulted in ultrastructural changes in atria, which can be attenuated by vitamin E co-administration.
Highlights
It is well established that long-term oral administration of amiodarone is extremely effective in the management of most supraventricular and ventricular tachyarrhythmias [1, 2]
The aim of this study is to test the adverse effects of amiodarone administration on cardiomyocytes and to study the possible protective role of vitamin E co-administration
Administration of amiodarone alone modified the atrial architecture, which was demonstrated by the following: mitochondrial enlargement and cristae lysis; marked heterogeneity of myofibril patterns with partial necrosis and disintegration of myofilaments; and irregularities of the sarcomere and less concentration of atrionatriuretic factor (ANF) granules, which localised in closed proximity to the nucleus with disrupted chromatin contents
Summary
It is well established that long-term oral administration of amiodarone is extremely effective in the management of most supraventricular and ventricular tachyarrhythmias [1, 2]. Amiodarone is categorised as a class III antiarrhythmic agent, as it prolongs the atrial and ventricular action potential duration (APD) as well as the refractory period of cardiac muscle. These effects are potentiated when the drug is given for longer durations [3]. Intravenous administration of amiodarone in studies conducted on dogs resulted in considerable reduction of myocardial contractility [6, 7] In spite of these advantages, adverse effects caused by amiodarone are frequent and can be serious and even lethal. The use of amiodarone is associated with ultrastructural changes affecting body tissues, but its effect on the ultrastructure of the heart has not yet been fully elucidated
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