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目的研究外燥对小鼠肺组织超微结构影响的病理特征。方法昆明种小鼠42只(SPF级)随机分为常温常湿组(A组)、温燥组(B组)、凉燥组(C组),每组14只;按文献条件造模处理后第6天、第12天电镜观察肺呼吸膜与Ⅱ型肺泡细胞(ATⅡ)超微结构;检测二棕榈酰卵磷脂(DPPC)含量。结果与A组比较,B组、C组第6、第12天肺呼吸膜增厚、肺泡隔增宽与弹性纤维组织增生;ATⅡ微绒毛减少与线粒体肿胀、嗜锇性板层小体(OMB)“平均面积”减小(P<0.05)伴DPPC持续下降(P<0.01)。结论肺呼吸膜增厚与纤维组织增生是燥证咳喘之证的超微组织病理学基础,提出ATⅡ之嗜锇性板层小体与线粒体结构异常可作为外燥伤肺病机的特异性超微病理学指标。
OBJECTIVE To study the pathological features of the ultrastructure of lung in mice induced by external dryness. Methods 42 Kunming mice (SPF grade) were randomly divided into normal temperature and humidity group (group A), warm dry group (group B) and cool dry group (group C), 14 in each group. On the 6th day and the 12th day, the ultrastructure of lung respiratory membrane and type Ⅱ alveolar cells (ATⅡ) were observed under electron microscope. The content of dipalmitoyl lecithin (DPPC) was detected. Results Compared with group A, the respiration membrane thickening, alveolar septum widening and elastic fiber tissue hyperplasia were observed on the 6th and 12th day in group B and group C; ATⅡ microvilli and mitochondria swelling, osmiophilic lamellar body (OMB ) “Mean area” decreased (P <0.05) with DPPC continued to decline (P <0.01). Conclusions Pulmonary respiratory membrane thickening and fibrous tissue hyperplasia are the basis of ultrastructure and histopathology of syndromes of dryness and cough and asthma. It is suggested that the osmiophilic lamellar bodies and mitochondrial structural abnormalities of AT Ⅱ may be used as specific super-dry-lung injury pathogens Micro-pathology indicators.