Abstract:
:Although amiodarone is a highly efficacious antidysrhythmic agent, the drug produces numerous adverse effects. The most critical of these is pulmonary toxicity because of the potential for mortality. This review examines the experimental model systems used to study amiodarone toxicity, summarizes the current state of knowledge regarding the processes involved in amiodarone-induced pulmonary toxicity (AIPT), and includes a discussion of potential future directions. Possible contributing processes to initiation of AIPT include phospholipidosis, altered calcium ion regulation, generation of reactive oxygen species, formation of an amiodarone aryl radical, and perturbation of cellular energy production. In addition, an immune response to the parent compound or to a metabolite could play a role. It is expected that elucidation of the mechanism(s) of AIPT will lead to safer antidysrhythmic agents and (or) to effective treatments for the prevention or amelioration of AIPT.
journal_name
Can J Physiol Pharmacoljournal_title
Canadian journal of physiology and pharmacologyauthors
Massey TE,Leeder RG,Rafeiro E,Brien JFdoi
10.1139/y95-730subject
Has Abstractpub_date
1995-12-01 00:00:00pages
1675-85issue
12eissn
0008-4212issn
1205-7541journal_volume
73pub_type
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journal_title:Canadian journal of physiology and pharmacology
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