DEXAMETHASONE PROTECTS HAMSTERS FROM FIBROSIS BUT NOT INFLAMMATION INDUCED BY INTRATRACHEAL AMIODARONE

Abstract

The antiarrhythmic drug amiodarone (AD) m ay cause severe lung damage in human patients. Often these patients are treated with corticosteroids; the usefulness of steroids in alleviating AD-induced lung disease has never been adequately studied, however. Intratracheal instillation of AD to hamsters causes pulmonary inflammation and fibrosis. The objective of this study was to examine whether corticosteroid treatment protects hamsters from AD-induced pulm onary inflammation and fibrosis. Male Syrian ham sters were treated with dexamethasone or saline and then instilled with AD or saline. Dexam ethasone treatm ent blocked the AD-induced increase in lung hydroxyproline content, an index of fibrosis. Analysis of bronchoalveolar lavage fluid showed that dexamethasone partially blocked AD-induced increases in total cells, m acrophages, and eosinophils. Dexam ethasone did not protect against the increase in neutrophils associated with AD treatm ent; neutrophil influx is widely utilized as a marker of inflamm ation. Dexam ethasone also failed to block the increase in lavage fluid albumin resulting from AD treatment; albumin in lavage fluid is considered an index of alveolar-capillary permeability. This study demonstrates that dexamethasone prevents AD-induced pulmonary fibrosis in hamsters while having m inim al effects on inflam mation.