Likhaechev Iu P, Batsura Iu D, Direev V I
Arkh Patol. 1975;37(2):63-9.
The article deals with results of morphological and electron-microscopy studies of the lungs in experimental pulmonary alveolar proteinosis in rats. The disease was reproduced in experiments on 500 animals by means of chronic inhalation of electro-welding copper-containing aerosols, condensations (smokes) which may develop under similar concentrations during electric welding. The lungs were investigated at intervals ranging from several days to two years from the beginning of the experiment, the duration of which was 9 months, the dayly exposure of the animals in inhalation cameras being three hours. The intra-alveolar content was composed of products of accelerated life activity of the cells of the alveolar epithelium as well as of perished phagocytes (proteins, lipids). The degree of manifestation of the process depended upon concentration of aerosol and duration of the experiment. In the zones of pulmonary alveolar proteinosis there were observed thickenings of the basal membranes, sclerosis of interalveolar partitions, slow replacement of perished macrophages by new ones, which were the causes of prolonged resolution of the alveols content. Pulmonary alveolar proteinosis (lipoproteinosis) should not be considered as a variety of pneumonia or edema of alveols.
本文探讨了大鼠实验性肺泡蛋白沉积症肺部的形态学和电子显微镜研究结果。通过长期吸入电焊含铜气溶胶、冷凝物（烟雾）在500只动物身上复制了该疾病，在电焊过程中，在类似浓度下可能会产生这些物质。从实验开始起，每隔几天到两年对肺部进行检查，实验持续9个月，动物每天在吸入舱内暴露3小时。肺泡内的物质由肺泡上皮细胞加速生命活动的产物以及死亡的吞噬细胞（蛋白质、脂质）组成。该过程的表现程度取决于气溶胶浓度和实验持续时间。在肺泡蛋白沉积症区域观察到基底膜增厚、肺泡间隔硬化、死亡巨噬细胞被新巨噬细胞缓慢替代，这是肺泡内容物长期消散的原因。肺泡蛋白沉积症（脂蛋白沉积症）不应被视为肺炎或肺泡水肿的一种类型。
