Auswirkung einer inhalativen Stickstoffdioxidexposition der Ratte auf die pulmonalen Alveolarsepten unter besonderer Berücksichtigung des extrazellulären Fasergerüstes
Die COPD ist eine weltweit verbreitete Erkrankung. Als Hauptursache gilt das Zigarettenrauchen. Bislang existiert keine Therapie, mit der sich die durch die COPD verursachten morphologischen und funktionellen Schäden an der Lunge rückgängig machen lassen. Die Forschung an Tiermodellen zielt nebe...
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Format: | Doctoral Thesis |
Language: | German |
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Philipps-Universität Marburg
2008
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Online Access: | PDF Full Text |
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Chronic Obstructive Pulmonary Disease (COPD) constitutes a worldwide problem, mainly caused by smoking. At present COPD lacks therapeutic options to ameliorate the morphological and functional changes to lung tissue associated with the disease. The elucidation of COPD pathogenesis and the testing of potential treatment strategies require the development of an animal model. To this extent the following study was undertaken. Male Fisher 344 Rats were exposed to 10 ppm of nitrogen dioxide for 3 or 21 days. The lungs of exposed animals were examined by transmission electron microscopy and compared to tissues of rats lacking nitrogen dioxide exposure. The assay focused on the ultrastructure of alveolar walls, including extracellular fibres. We observed inflammation, indicated by and increased number of alveolar macrophages and increased alveolar volume, established by an increase in type II pneumocytes after three days of NO2 treatment. After 21 days of exposure we saw a change in the composition of extracellular fibres. However, we did not observe any signs of emphysema. Furthermore, the capillary endothelium appeared unchanged. However, the NO2 exposed animals also consumed significantly less food than the control group. Whether the detected differences stem from nitrogen dioxide exposure or were secondary to reduced food consumption could not be determined.