Amiodarone 為第一線的抗心律不整用藥，會引起不同的副作用，其中肺毒性是最嚴重且具致命性，但機轉不詳。Amiodarone 引起之肺病理反應包括肺通透性的改變、肺泡出血、肺泡炎、以及最終形成肺纖維化。Amiodarone 引起肺纖維化的可能機轉包括: 1) 自然殺手細胞參與引起肺內局部的免疫反應；2) 氧游離基的釋出以及激活的白血球，淋巴球或酸性球聚集在肺內；3) Amiodarone 抑制了許多細胞內的酯，以致磷脂質累積；4) 肺纖維化與各種細胞素TNF 、TGF 1、IL4、IL8、等有關。其中NF B 之活化扮演著重要角色；5) Amiodarone 可誘發肺泡上皮細胞的凋亡而此作用與Angiotensin II 有關；6) Amiodarone 會增加肺沖洗液內白蛋白，乳酸去氫、吞噬細胞、嗜中性白血球、嗜酸性白血球以及過氧 (myloperoxidase)。由於Amiodarone 在臨床的應用愈來愈廣，Amiodarone 引發之肺毒性病例勢必增加。因此，服用Amiodarone 患者應該週期性的做肺功能檢查、支氣管鏡檢查、肺沖洗液、活體切片或肺瀰散量等不同的測定。

Amiodarone is a first-line antiarrthythmic agent which caninduce different side effects; lung toxicity can be fatal but the mechanisms involved are not yetclear. Amiodarone-induced lung pathological changes including permeability changes, alveolarhemorrhage, alveolitis and lung fibrosis. There are several mechanisms involved in lung fibrosis: 1)activation of natural killer cells and induction of an immune response; 2) release of oxygen radicalsand activation of sequestered white cells, lymphocytes and eosinophils; 3) inhibition ofintracellular phospholipases so that phospholipids accumulation; 4) the involvement of cytokinessuch as tumor necrotic factor , transforming growth factor (1, interleukin (IL) 4, IL8; 5) inductionof apoptosis of alveolar cell in which angiotensin II is involved; and 6) increase in lavage albumin,lactic dehydrogenase, macrophages, neutrophils, eosinophils, and myloperoxidase increased. Sincecases of lung fibrosis increase with increased utilization of amiodarone, regular pulmonaryfunction tests, bronchoscopic examinations, lung lavage, biopsies and diffusing capacitymeasurement are necessary.