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The effects of vitamin E deficiency on bleomycin (BLM)-induced pulmonary fibrosis have been studied by analyses of pressure volume (PV) curves and morphological examinations. Golden hamsters were divided into groups on a control diet (group C), vitamin E-deficient diet (E), control diet with BLM treatment (CB), and vitamin E-deficient diet with BLM treatment (EB). Group EB showed PV curves shifted downward and to the right soon after BLM administration (10 days) and gradually shifted upward and to the left compared to group CB in the later period (30 and 60 days after BLM treatment). Histologically group EB was characterized by relatively severe interstitial pneumonitis in the early stages. In later stages, emphysematous changes were induced in combination with a lesser degree of fibrosis in group EB. Mean thickness of the alveolar wall of group CB was larger than group C while that of group EB was smaller at 30 days after BLM treatment. These results indicate that, with BLM treatment, vitamin E-deficient hamsters show increased distensibility on the PV curve and emphysematous changes mixed with focal fibrosis on morphological examination. This means that by adding other modulating factors, such as vitamin E deficiency, BLM, an agent known to produce pulmonary fibrosis, acts to induce an emphysematous lesion in the lung. Although pulmonary fibrosis and emphysema have been considered to be final and different forms of parenchymal injury, each may proceed to the other under the influence of some modulating factors.
The effects of vitamin E deficiency on bleomycin (BLM)-induced pulmonary fibrosis have been studied by analyses of pressure volume (PV) curves and morphological examinations. Golden hamsters were divided into groups on a control diet (group C), vitamin E-deficient diet (E), control diet with BLM treatment (CB), and vitamin E-deficient diet with BLM treatment (EB). Group EB showed PV curves shifted downward and to the right soon after BLM administration (10 days) and gradually shifted upward and to the left compared to group CB in the later period (30 and 60 days after BLM treatment). Histologically group EB was characterized by relatively severe interstitial pneumonitis in the early stages. In later stages, emphysematous changes were induced in combination with a lesser degree of fibrosis in group EB. Mean thickness of the alveolar wall of group CB was larger than group C while that of group EB was smaller at 30 days after BLM treatment. These results indicate that, with BLM treatment, vitamin E-deficient hamsters show increased distensibility on the PV curve and emphysematous changes mixed with focal fibrosis on morphological examination. This means that by adding other modulating factors, such as vitamin E deficiency, BLM, an agent known to produce pulmonary fibrosis, acts to induce an emphysematous lesion in the lung. Although pulmonary fibrosis and emphysema have been considered to be final and different forms of parenchymal injury, each may proceed to the other under the influence of some modulating factors.
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