Browsing by Author "Oyarzun, M"

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    Bleomycin-induced chronic lung damage does not resemble human idiopathic pulmonary fibrosis
    (AMER THORACIC SOC, 2001) Borzone, G; Moreno, R; Urrea, R; Meneses, M; Oyarzun, M; Lisboa, C
    Administration of bleomycin into the lungs of experimental animals has been utilized as a model to understand human pulmonary fibrosis. Most of the studies, however, have focused on early stages of the lung reaction. We hypothesized that chronic stages of the model may not mimic idiopathic pulmonary fibrosis, since in preliminary studies, lung volume and compliance were not decreased. Eight male Sprague-Dawley rats receiving intratracheal bleomycin (0.5 U/100 g body weight) underwent measurement of FRC, inspiratory capacity, and lung compliance 120 d later. Lung histologic changes were evaluated using light microscopy. Eight rats without intervention served as controls. Results show that our model, in early stages, has histologic changes no different from those previously described elsewhere. In chronic stages, however, the model does not behave as a restrictive syndrome: FRC is normal or increased, whereas lung compliance is normal. Focal peribronchiolar inflammation and fibrosis associated with paracicatricial emphysematous changes are the main histologic features of long-term lung remodeling after bleomycin. We conclude that while the chronic stages of the model may be informative in understanding mechanisms of fibrosis, care should be taken not to extrapolate to human idiopathic pulmonary fibrosis. We speculate that the model might resemble a particular subgroup of human interstitial lung disease, namely, those involving peribronchiolar structures.
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    Effect of 0.25 ppm Ozone exposure on. pulmonary damage induced by bleomycin
    (SOCIEDAD BIOLGIA CHILE, 2005) Oyarzun, M; Dussaubat, N; Gonzalez, S
    To study the effect of ozone in a chronically damaged lung. we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O-3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O-3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O-3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (IU/100 g body weight) and, 30 days later, exposed to 0.25 ppm O-3 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O-3 exposure. BLM-induced lung damage did not change after 60 days of days of O-3 exposure. Five days of O-3 exposure increased the mean score of BLM-induced pulmonary suggesting that a short-term exposure to O-3 in a previously damaged lung might be a risk factor for developing further lung injury.