ABSTRACT
Pulmonary fibrosis is characterized by having changes in lung connective tissue distribution and content. Amiodarone, a benzofuran, is capable of causing pulmonary fibrosis in hamsters after a single intratracheal treatment. Morphological studies indicate that collagen is altered in both human lung fibrosis and animal models of this disease. The elastin component has been found to be elevated in animal models of interstitial lung disease. Examination of the amiodarone model of pulmonary fibrosis reveals that there are a number of events which lead to an end-stage lung. These events fulfill the four basic criteria which any experimental model of lung fibrosis must meet: inflammation, cellular proliferation, increased matrix synthesis, and lung remodeling. The earliest stage of the injury process involves an acute inflammatory reaction. Cell proliferation occurs in the epithelial compartment which is associated with cell injury and replacement.
