Barth P J, Uhlarik S, Bittinger A, Wagner U, Rüschoff J
Department of Pathology, Philipps-Universität Marburg/Lahn, Germany.
Pathol Res Pract. 1994 Jan;190(1):33-41. doi: 10.1016/s0344-0338(11)80494-2.
In order to quantify parenchymal, vascular and epithelial changes occurring in the exudative and organizing phase of diffuse alveolar damage (DAD) induced by inhaled NO2 groups of 7 rats were continuously exposed to 5, 10 or 20 ppm NO2 for 3 and 25 days alternatively. AgNOR analysis revealed the highest proliferative activity in the epithelium of the respiratory bronchioles. In this region already after 3d exposure to 5 ppm the maximum AgNOR number was reached. In contrast to long-term exposure after 3d exposure to 5 and 10 ppm NO2 the AgNOR number in the respiratory bronchioles was significantly higher than in central airway epithelia. After long-term exposure to 5 and 10 ppm AgNOR number decreased to normal values or showed no further significant increase, long-term exposure to 20 ppm resulted in a further increase of the AgNOR number. A significant increase of the alveolar circumference and decrease of alveolar surface density was found after an exposure to 20 ppm for 3d and long-term exposure to 10 and 20 ppm NO2, whereas the 5 ppm exposure groups disclosed no significant change of these values. Medial hypertrophy was detected after exposure to 10 and 20 ppm NO2 for 25 days, after the exposure to 5 ppm for 3d and 25d medial thickness was significantly decreased due to vasodilation induced by NO, one of the major reaction products of NO2.
为了量化吸入二氧化氮（NO₂）诱导的弥漫性肺泡损伤（DAD）渗出期和机化期实质、血管和上皮的变化，将7只大鼠分为一组，交替连续暴露于5、10或20 ppm的NO₂中3天和25天。AgNOR分析显示呼吸细支气管上皮细胞增殖活性最高。在该区域，暴露于5 ppm的NO₂ 3天后就达到了最大AgNOR数量。与长期暴露不同，暴露于5和10 ppm的NO₂ 3天后，呼吸细支气管中的AgNOR数量显著高于中央气道上皮细胞。长期暴露于5和10 ppm后，AgNOR数量降至正常值或无进一步显著增加，长期暴露于20 ppm导致AgNOR数量进一步增加。暴露于20 ppm的NO₂ 3天以及长期暴露于10和20 ppm的NO₂后，肺泡周长显著增加，肺泡表面密度降低，而暴露于5 ppm的组这些值无显著变化。暴露于10和20 ppm的NO₂ 25天后检测到中膜肥厚，暴露于5 ppm的NO₂ 3天和25天后，由于NO₂的主要反应产物之一NO诱导的血管舒张，中膜厚度显著降低。
