Merchant R K, Peterson M W, Hunninghake G W
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
J Appl Physiol (1985). 1990 Apr;68(4):1354-9. doi: 10.1152/jappl.1990.68.4.1354.
Alveolar epithelial cell injury and increased alveolar-capillary membrane permeability are important features of acute silicosis. To determine whether silica particles contribute directly to this increased permeability, we measured paracellular permeability of rat alveolar epithelium after exposure to silica, in vitro, using markers of the extracellular space. Silica (Minusil) markedly increased permeability in a dose- and time-dependent manner. This was not the result of cytolytic injury, because lactate dehydrogenase release from monolayers exposed to silica was not increased. Pretreatment of the silica with serum, charged dextrans, or aluminum sulfate blocked the increase in permeability. Scanning electron microscopy demonstrated adherence of the silica to the surface of the alveolar epithelial cells. Thus silica can directly increase permeability of alveolar epithelium.
肺泡上皮细胞损伤和肺泡-毛细血管膜通透性增加是急性矽肺的重要特征。为了确定二氧化硅颗粒是否直接导致这种通透性增加,我们在体外使用细胞外空间标记物测量了大鼠肺泡上皮细胞在接触二氧化硅后的细胞旁通透性。二氧化硅(Minusil)以剂量和时间依赖性方式显著增加通透性。这不是细胞溶解损伤的结果,因为暴露于二氧化硅的单层细胞中乳酸脱氢酶的释放并未增加。用血清、带电荷的葡聚糖或硫酸铝预处理二氧化硅可阻断通透性的增加。扫描电子显微镜显示二氧化硅粘附在肺泡上皮细胞表面。因此,二氧化硅可直接增加肺泡上皮的通透性。