Shanker R, Dogra R K, Sahu A P, Zaidi S H
Arch Toxicol. 1976 Oct 28;36(2):151-7. doi: 10.1007/BF00351975.
Experimental manganese lymphadenopathy was produced by guinea pigs by intratracheal inoculation of manganese dioxide (50 mg/300 g body weight) and histopathologic changes in the tracheobronchial lymph nodes were studied up to 180 days. There was slow extracellular transport of manganese dust into the nodes, which did not provoke any significant reaction at early periods. However, at later periods the nodes exhibited a significant increase in the density of dust particles and the reaction consisted of phagocytosis, degeneration of dust laden macrophages, slight proliferation of fibroblasts, together with some reticulinosis corresponding to deposits of dust particles. The significance of these findings have been discussed from the chronic toxicity viewpoint.
通过气管内接种二氧化锰（50毫克/300克体重）在豚鼠身上诱发实验性锰淋巴结病，并对气管支气管淋巴结的组织病理学变化进行了长达180天的研究。锰尘向淋巴结的细胞外转运缓慢，在早期未引发任何明显反应。然而，在后期，淋巴结中尘粒密度显著增加，反应包括吞噬作用、载尘巨噬细胞变性、成纤维细胞轻度增生，以及与尘粒沉积相应的一些网状纤维增生。已从慢性毒性角度讨论了这些发现的意义。
