OBJECTIVE: To study the effects of short-term exposure to high oxygen concentrations (hyperoxia) on Wistar rat lungs. METHODS: Animals were divided into three groups exposed to hyperoxia for 10', 30' and 90' (O10', O30', O90', respectively), together with a control group (exposed to room air). The animals were sacrificed 24 h after exposure. Bronchoalveolar lavage was performed, and the lungs were removed for histological and stereological analysis. RESULTS: In the O10', O30', and O90' groups, respectively and in comparison with the controls, we observed an increase in the numbers of macrophages (2169.9 +/- 118.0, 1560.5 +/- 107.0, and 1467.6 +/- 39.0 vs. 781.3 +/- 78.3) and neutrophils (396.3 +/- 35.4, 338.4 +/- 17.3, and 388.7 +/- 11.7 vs. 61.6 +/- 4.2), concomitant with an increase in oxidative damage (143.0 +/- 7.8%, 180.4 +/- 5.6%, and 235.0 +/- 13.7 vs. 100.6 +/- 1.7%). The histological and stereological analyses revealed normal alveoli and alveolar septa in the controls (83.51 +/- 1.20% and 15 +/- 1.21%), in the O10' group (81.32 +/- 0.51% and 16.64 +/- 0.70%), and in the O30' group (78.75 +/- 0.54% and 17.73 +/- 0.26%). However, in the O90' group, inflammatory cell infiltration was observed in the alveoli and alveolar septa. Red blood cells extravasated from capillaries to the alveoli (59.06 +/- 1.22%), with evidence of congestion, hemorrhage, and septal edema (35.15 +/- 0.69%). CONCLUSION: Hyperoxia for 90' caused injury of the lung parenchyma, resulting in oxidative damage and inflammatory cell infiltration.
OBJECTIVE: To study the effects of short-term exposure to high oxygen concentrations (hyperoxia) on Wistar rat lungs. METHODS: Animals were divided into three groups exposed to hyperoxia for 10', 30' and 90' (O10', O30', O90', respectively), together with a control group (exposed to room air). The animals were sacrificed 24 h after exposure. Bronchoalveolar lavage was performed, and the lungs were removed for histological and stereological analysis. RESULTS: In the O10', O30', and O90' groups, respectively and in comparison with the controls, we observed an increase in the numbers of macrophages (2169.9 +/- 118.0, 1560.5 +/- 107.0, and 1467.6 +/- 39.0 vs. 781.3 +/- 78.3) and neutrophils (396.3 +/- 35.4, 338.4 +/- 17.3, and 388.7 +/- 11.7 vs. 61.6 +/- 4.2), concomitant with an increase in oxidative damage (143.0 +/- 7.8%, 180.4 +/- 5.6%, and 235.0 +/- 13.7 vs. 100.6 +/- 1.7%). The histological and stereological analyses revealed normal alveoli and alveolar septa in the controls (83.51 +/- 1.20% and 15 +/- 1.21%), in the O10' group (81.32 +/- 0.51% and 16.64 +/- 0.70%), and in the O30' group (78.75 +/- 0.54% and 17.73 +/- 0.26%). However, in the O90' group, inflammatory cell infiltration was observed in the alveoli and alveolar septa. Red blood cells extravasated from capillaries to the alveoli (59.06 +/- 1.22%), with evidence of congestion, hemorrhage, and septal edema (35.15 +/- 0.69%). CONCLUSION:Hyperoxia for 90' caused injury of the lung parenchyma, resulting in oxidative damage and inflammatory cell infiltration.
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