Effects of In Vitro Amiodarone Exposureon Alveolar Macrophage Inflammatory Mediator Production
The American Journal of the Medical Sciences, ISSN: 0002-9629, Vol: 304, Issue: 6, Page: 352-356
1992
- 13Citations
- 3Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef6
- Captures3
- Readers3
Article Description
Administration of amiodarone, although often lifesaving, is associated with pulmonary side effects. Patients with amiodarone pulmonary toxicity can present with either a chronic disorder that suggests pulmonary fibrosis or a more acute process. Mechanisms of acute pulmonary injury resulting from amiodarone are unclear. Previous studies have demonstrated that the drug is preferentially concentrated in alveolar macrophages. In the present study, the authors examined whether in vitro exposure to amiodarone resulted in alteration of rat alveolar macrophage superoxide, leukotriene B 4, or fibronectin release. In addition, the authors assessed whether macrophages were ultrastructurally altered by in vitro amiodarone exposure. Twenty four hour exposure to therapeutic tissue concentrations of amiodarone resulted in enhancement of phorbol myristate acetate-stimulated macrophage superoxide release. In addition, 48 hours exposure to amiodarone caused a dose-dependent inhibition of spontaneous fibronectin release by macrophages. Macrophages exposed to 48 hours of 10 μ g/ml amiodarone were ultrastructurally abnormal, containing lamellar inclusions and demonstrating a large degree of vacuolization. The authors concluded that alveolar macrophages are very sensitive to therapeutic tissue concentrations of amiodarone. Alteration of macrophage mediator release by amiodarone may be one mechanism for lung damage induced by the drug.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0002962915355865; http://dx.doi.org/10.1097/00000441-199212000-00004; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0027051092&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/1333729; https://linkinghub.elsevier.com/retrieve/pii/S0002962915355865; https://dx.doi.org/10.1097/00000441-199212000-00004
Elsevier BV
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