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目的模拟矽肺的致病过程,建立初步的矽肺犬动物模型。方法利用气管插管及呼吸机通气,将二氧化硅粉末吹入实验犬肺内,观察不同染尘剂量、不同染尘频次下,各持续时间段内(染尘前,染尘1、2、3个月)实验犬的动脉血气、胸部CT影像学、肺组织病理形态学改变。结果各组实验犬染尘前后的动脉血气水平无明显差异(P>0.05),但染尘后实验犬胸部CT均有不同程度的磨玻璃样改变,肺组织病理可见肺间质增厚,终末细支气管壁周围大量吞尘巨噬细胞聚集,有成纤维细胞增生及网状胶原纤维形成,偏光显微镜下可见肺间质内二氧化硅颗粒沉积,且染尘犬胸部CT及肺组织病理改变程度与染尘剂量、染尘频次、染尘时间呈正相关。结论经气管插管后呼吸机通气,每次按400 mg/kg称取二氧化硅粉尘吹入实验犬肺内,每周染尘1次,持续染尘3个月,可建立初步的矽肺犬动物模型。
Objective To simulate the pathogenesis of silicosis and establish a preliminary animal model of silicosis. Methods Using intratracheal intubation and ventilator ventilation, the silica powder was blown into the lungs of experimental dogs to observe the effects of different doses of dust, different frequency of dust and dust, 3 months) experimental arterial blood gas, chest CT imaging, pathological changes of lung tissue. Results There was no significant difference in arterial blood gas levels between experimental dogs before and after dying dust (P> 0.05). However, the chest CT showed varying degrees of ground-glass-like changes after lung exposure. A large number of phagocytic macrophages gathered around the fine bronchial wall fibroblasts and the formation of reticular collagen fibers, microscopic examination of lung interstitial deposition of silica particles, and Dust canine chest CT and lung tissue pathological changes The degree of dust dose, dust frequency, dust time was positively correlated. Conclusions The ventilator ventilated after tracheal intubation, each time by 400 mg / kg weighed silica dust into the lungs of experimental dogs, dust once a week, continued to dust for 3 months to establish a preliminary silicosis dogs Animal model