EJMS

Abstract

Background: Amiodarone (AMD) is an anti-arrhythmic agent that has potentially life threatening pulmonary adverse effects. The purpose of the present study is to explore the effects of AMD on alveolar epithelial cells and lung mesenchyme and the mechanism inducing these effects. Material and methods: Thirty adult male albino rats were divided into two equal groups. Control group and AMD group, given AMD 10 mg/kg/day orally for one month. The lungs were dissected, routine histological sections, immunohistochemical staining against tumor necrosis factor α (TNFα), ultrathin sections were prepared and morphometric measurements and statistical analysis were done. Results: The lungs in AMD-treated group showed marked congestion, interstitial haemorrhage, inflammatory cellular infiltration and pyknotic nuclei with many alveolar pneumocytes having vacuolated cytoplasm and hypertrophied obliterated arterioles were seen. The interalveolar septa revealed marked fibrotic changes with obliteration of the alveoli. AMD-treated group showed no difference in the TNFα immunoexpression from the control. Ultrastructurally, type ІІ pneumocytes showed hypertrophy with many expanded elongated microvilli, lamellated vacuoles with myelin figures and many inclusion body vacuoles. Multiple fat globules were seen in type І pneumocytes. Alveolar macrophages had excessive amount of inclusion body vacuoles within the interalveolar septa and inside the alveoli with increased collagen fibre deposition within the septa. Conclusion: AMD directly injured type ІІ pneumocytes and reduced their ability to form surfactant with enhancement of alveolar collapse and caused accumulation of lipid globules in type І cells. It stimulated inflammatory reaction with recruitment of tissue macrophages and interstitial pulmonary fibrosis impairing the air blood interface exchange barrier.