Conclusion The decrease of SP A and SP B in alveolar type II cells seems to play an important role in the development of emphysema. 结论实验性金黄地鼠肺气肿肺泡Ⅱ型上皮细胞内SPA和SPB明显减少可能是肺气肿发展的重要环节之一。
An Experimental Study of the Protective Action on Alveolar Macrophages of Pulmonary Emphysema by Bilirubin 胆红素对肺气肿肺泡巨噬细胞保护作用的实验研究
Conclusion The decrease of VEGF and KDR and the increase of alveolar septal cell apoptosis may contribute to the pathogenesis of emphysema. 结论VEGF及KDR水平减少与肺泡隔细胞凋亡的增加可能与肺气肿的发生相关。
Results: The alveolar pulmonary interstitium effusion, engorgement, emphysema are the main appearances of chest films for wet lung disease of neonatal. 结果:肺泡及肺间质积液、肺淤血、肺气肿等是新生儿湿肺症的重要X线征象。
Changes of surfactant A and B in alveolar type ⅱ cells in hamster with elastase induced emphysema 金黄地鼠实验性肺气肿肺泡Ⅱ型上皮表面活性物质蛋白A和B的变化
But there were obvious differences in the model group, such as narrowed alveolar space, thickened alveolar wall, lung congestion, pulmonary edema, infiltration of inflammatory cells, markedly increased of cavity tablets alveolar cells, and local emphysema. 模型组肺泡腔变窄,肺泡壁增厚;肺充血,肺间质水肿,可见炎细胞浸润,肺泡腔内可见粒细胞明显增多,并见局部肺气肿。
Light microscope ( HE): PQ group shows that focal pulmonary hemorrhage, alveolar wall thickening apparent, alveolar and interstitial pulmonary edema, inflammatory cell infiltration, and some sections can be seen focal atelectasis, emphysema. 光镜检查:PQ组可见肺灶性出血,肺泡壁明显增厚,肺泡和肺间质水肿,大量炎性细胞浸润,部分切片可见灶状肺不张,肺气肿。
These studies demonstrated that, at least in animal models, apoptosis of alveolar wall or endothelial cells is sufficient to cause pulmonary emphysema, even without the accumulation of inflammatory cells. 动物实验证明即使没有炎性细胞的聚集,肺泡壁细胞或内皮细胞凋亡也足够引起肺气肿的发生。