Cristi L. Ogle

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Treatment of humans with the antiarrhythmic drug, amiodarone (AD), may result in the development of pulmonary toxicity. To characterize this response, male Fischer 344 rats were treated with AD for 1, 3, 9, and 16 weeks. AD induces a twofold increase in the level of pulmonary phospholipid after 3 weeks of treatment. Continued administration results in only(More)
Administration of the antiarrhythmic drug amiodarone to humans or animals may result in lung damage. Amiodarone is metabolized to desethylamiodarone and other minor metabolites. Because amiodarone and the metabolites accumulate in the lungs, it is not possible to ascertain the role of each of these compounds in the induction of toxicity. In the present(More)
Humans treated with the antiarrhythmic drug amiodarone may develop pulmonary toxicity accompanied by the presence of alveolar macrophages (AM) containing lamellar inclusions. This cellular response is indicative of the development of a drug-induced phospholipidosis. To characterize this response of the AM, Fischer-344 rats were treated with amiodarone, and(More)
Treatment of humans with the antiarrhythmic drug amiodarone can cause pulmonary pathology and toxicity. The disorder is associated with the accumulation of phospholipid, amiodarone, and its principal metabolite desethylamiodarone in lung tissue. To better understand the response of the lung to amiodarone administration, the distribution of total(More)
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