Beta-aminopropionitrile prevents bleomycin-induced pulmonary fibrosis in the hamster

β-Aminopropionitrile (βAPN), an agent that prevents collagen accumulation in tissues, was evaluated for its ability to prevent excess collagen formation in bleomycin-induced pulmonary fibrosis in the hamster. Two groups of animals received a single endotracheal dose of bleomycin; ome of these was injected with βAPN twice daily for 30 days. A third group received endotracheal saline and a fourth group received saline and βAPN. After 30 days, we measured pressure-volume curves of saline-filled lungs, collagen content, and degree of fibrosis. Endotracheal bleomycin increased collagen content, decreased lung volume, and produced fibrosis and a mortality rate of 51%. The administration of βAPN to bleomycin treated animals prevented excess collagen accumulation and diminished total protein, reversed volume diminution, produced less fibrosis, and improve the mortality rate to 24%; βAPN alone had no effect on lung mechanics or collagen content. The biochemical, functional, and structural features of bleomycin induced lung fibrosis are amenable to control with βAPN.