Riley D J, Kerr J S, Berg R A, Ianni B D, Pietra G G, Edelman N H, Prockop D J
Am Rev Respir Dis. 1982 Jan;125(1):67-73. doi: 10.1164/arrd.1982.125.1.67.
beta-Aminopropionitrile (beta APN), 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; one of these was injected with beta APN twice daily for 30 days. A third group received endotracheal saline and a fourth group received saline and beta APN. 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 beta APN to bleomycin-treated animals prevented excess collagen accumulation and diminished total protein, reversed volume diminution, produced less fibrosis, and improved the mortality rate to 24%; beta APN 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 beta APN.
β-氨基丙腈(β-APN)是一种可阻止组织中胶原蛋白积累的药物,我们对其预防仓鼠博来霉素诱导的肺纤维化中过量胶原蛋白形成的能力进行了评估。两组动物接受了单次气管内博来霉素给药;其中一组每天注射两次β-APN,持续30天。第三组接受气管内生理盐水,第四组接受生理盐水和β-APN。30天后,我们测量了充满生理盐水的肺的压力-容积曲线、胶原蛋白含量和纤维化程度。气管内注射博来霉素增加了胶原蛋白含量,减小了肺容积,并产生了纤维化,死亡率为51%。给接受博来霉素治疗的动物施用β-APN可防止过量胶原蛋白积累,减少总蛋白,逆转容积减小,产生较少的纤维化,并将死亡率提高到24%;单独使用β-APN对肺力学或胶原蛋白含量没有影响。博来霉素诱导的肺纤维化的生化、功能和结构特征可用β-APN进行控制。