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为观察甲苯二异氰酸酯 (TDI)吸入引起的肺损伤 ,将 30只小鼠均分为 5组 ,分别吸入 4.30± 0 .6 0mg·m 3 TDI 0～ 4周 ,常规留取病理及电镜标本。实验结果显示 :TDI吸入早期肺间质局灶性增生、水肿 ,小气道及血管周围大量淋巴细胞及嗜酸性粒细胞浸润。TDI吸入后 3周 ,肺间质弥漫性增生 ,部分肺组织有炎性肉芽肿形成及肺实变 ,间质增生以弹力纤维及网状纤维增生为主。扫描电镜示气道上皮细胞纤毛脱落 ,气管腔内炎性细胞渗出 ,TDI吸入早期分泌细胞功能亢进 ,晚期功能低下。透射电镜示Ⅱ型肺泡上皮及肺毛细血管基底膜增生 ,血管内皮电子密度增加 ,线粒体肿胀。以上结果提示 :吸入TDI可引起小鼠肺内多方面损伤。
To observe the lung injury induced by toluene diisocyanate (TDI) inhalation, all 30 mice were divided into 5 groups and were respectively infused with 4.30 ± 0.60 mg · m 3 TDI for 0 to 4 weeks. Pathological and electron microscopic specimens were routinely collected. The experimental results showed that: TDI inhaled early pulmonary interstitial focal hyperplasia, edema, small airways and a large number of perivascular lymphocytes and eosinophil infiltration. Three weeks after TDI inhalation, interstitial diffuse hyperplasia, some of the lung tissue with inflammatory granuloma formation and lung consolidation, interstitial hyperplasia mainly elastic fibers and reticular fibrosis. Scanning electron microscopy showed airway epithelial cells cilia shedding, tracheal cavity inflammatory cell exudation, TDI inhaled early secretory cell hyperthyroidism, advanced dysfunction. Transmission electron microscopy showed type II alveolar epithelial and pulmonary capillary basement membrane hyperplasia, vascular endothelial electron density increased, mitochondria swelling. The above results suggest that: inhaled TDI can cause multiple lung damage in mice.