Quantitativ-histologische Untersuchung der Auswirkungen einer inhalativen Stickstoffdioxid-Exposition der Maus – Einfluss von Expositionsdauer und Lebensalter

Die NO2 Exposition von Mäuselungen wird bisweilen als Tiermodell der Emphysementstehung im Rahmen der Forschung über das Chronic Obstructive Pulmonary Disease (COPD) angesehen und eingesetzt. In dieser Arbeit wurde der Einfluss der Faktoren „Alter“ und „Dauer der NO2-Exposition“ untersucht. Hierzu...

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Bibliographic Details
Main Author: Landenberger, Barbara
Contributors: Fehrenbach, Heinz (Prof. Dr.) (Thesis advisor)
Format: Doctoral Thesis
Published: Philipps-Universität Marburg 2008
Online Access:PDF Full Text
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The NO2 exposition of mouse lungs is used as animal model for developement of emphysema within the research about the Chronic Obstructive Pulmonary Disease (COPD). In this work the influence of the factors "age" and "time of exposition" was examined. Two groups of different aged C57BL/6mice (1,5-2 months or 12 months) were selected and then exposed to stickstoffdioxide during 25days. Their lungs were compared with animals same to age who were held in space air. In addition, the young animals were exposed to two differently long exposition times (25 or 55 days). The appearance of a pulmonary emphysema was judged with the help of stereological methods. On this occasion, the structural parametres which permit statements about "airspace enlargement" and loss of septal volume, both sign of an emphysema development, were determined. For the proof of "airspace enlargement" served the determinaton of the volume-weighted mean volume of the parenchymal airspaces and the Mean Chord Length. A loss of septa should be proved about the loss of alveolar surface area and septal volume. As a result an enlargement of the airspace appeared by NO2 exposition. The volume-weighted mean volume of the parenchymal airspaces was raised in the test groups of the young animals towards the controlling animals significantly, the Mean Chord Length (CM) produced no significant differences between exposition groups and control groups. A decrease of alveolar surface area within the NO2-exposed groups which is expected with emphysema development didnt happen. The alveolar surface area was bigger within the exposition groups than within the controlling animals, also the septal volume. A higher sensitivity of the young animals towards NO2 exposition compared to adults was detected. Young mice demonstrated a significantal enlargement of the alveolar width after exposition. Against it there was no significant exposition-conditioned difference in the alveolar width of the controlling group and test group within the older animals. Same proved the determination of lung volume and surface density. Another aspect of this work was the investigation of the controlling mouse lungs in regard to the development of a physiological aged emphysema. An airspace enlargement without loss of alveolar septs was dected as well. Mean Chord Length (CM), alveolar surface aera, septal volumes and lung volumes were raised significantly within the old animals towards the young animals. The NO2 exposition to C57BL/6 mice is no suitable model for the development of emphysema as a sign of the COPD. Also different exposition times as well as a different age of the animals at exposition time had no significant influence on the development of emphysema.