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机构地区:[1]南方医科大学珠江医院儿科,广东广州510282 [2]北京军区总医院病理科 [3]北京军区总医院八一儿童医院
出 处:《中国妇幼保健》2009年第18期2544-2547,共4页Maternal and Child Health Care of China
基 金:国家自然科学基金项目(30772036)
摘 要:目的:观察实验性支气管肺发育不良小鼠的肺部病变。方法:将30只4日龄雌性昆明种小鼠随机分为两组,每组15只,实验组置于氧箱中(FiO20.6),对照组置于空气中(FiO20.21),分别于实验第7天、第14天、第21天时分离小鼠肺组织,观察病理形态、超微结构及肺胶原含量变化。结果:实验组HE染色下见正常肺泡结构消失、肺泡融合、肺泡间隔增厚,放射状肺泡计数(radical alveolar counts,RAC)较对照组明显减少(P<0.001),天狼猩红特殊染色见肺Ⅰ型、Ⅲ型胶原增生,与对照组相比胶原面积显著增加(P<0.001),电镜下见板层小体及微绒毛减少。结论:持续较高浓度氧吸入可致新生小鼠发生类似人类支气管肺发育不良的肺部改变。Objective: To observe the pulmonary lesions of rats with bronchopulmonary dysplasia. Methods: 30 4 - days - old female rats were divided into control group ( FiO20. 21, n = 15 ) and model group ( FiO20. 6, n = 15 ) randomly. Pathomorphological changes, uhramicrostucture and collagen level were detected on the seventh days, fourteenth days and twenty - first days after experiment. Results: Stained by HE, lungs of model group showed destroy of alveoli, alveoli fusion and increased septal wall thickness, radical alveolar counts were significantly lower than those in model group (P 〈0. 001 ) . Stained by sirius rosebb, the expression levels of collagen Ⅰ and collagen Ⅲ increased, collagen area was significantly higher than that of control group (P 〈 0. 001 ) . Lamellar bodies and microvilli of model group decreased under electron microscope. Conclusion: Long - term exposure to oxygen of high concentration can induce bronchopulmonary dysplasia - like lesions in lung structure of rats.
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