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目的探讨先天性膈疝(CDH)肺发育不良的机制,研究CDH模型胎鼠肺组织不同发育阶段的超微结构特点。方法将7只Sprague-Dawley(SD)孕鼠用随机数字表法分为两组,膈疝组(n=4):于孕9.5 d用Nitrofen(125 mg/只,溶于2 ml橄榄油中)灌胃1次,分别于SD鼠孕16 d1、8 d和21 d取胎鼠3只、10只、17只;对照组(n=3):于妊娠9.5 d时用橄榄油2 ml灌胃1次,分别于SD鼠孕16 d、18 d和21 d各取胎鼠10只。将16 d胎鼠肺组织切片进行透射电子显微镜观察;18 d胎鼠肺组织进行HE染色,透射电子显微镜观察并统计膈疝的发生率;21 d胎鼠肺组织除进行HE染色、透射电子显微镜观察、统计膈疝的发生率外,计算胎鼠肺重与体重比(Lw/Bw)。结果 (1)膈疝组胎鼠肺重/体重比显著低于对照组(0.0238 vs.0.0430,P=0.04);膈疝组18 d和21 d时胎鼠膈疝发生率分别为90.00%和82.35%,表明膈疝组胎鼠肺发育不良,而对照组18 d和21 d时胎鼠均无膈疝发生;(2)与对照组相比,膈疝组16 d时胎鼠肺超微结构也呈现出肺发育不良的改变:基板较宽,内容物很少;肺上皮细胞常染色质为主,核糖体丰富;支气管腔无微绒毛;18 d和21 d的样品观察表明,随着孕期的延长,上述特征更明显;(3)对照组与膈疝组孕21 d时胎鼠肺泡Ⅱ型上皮细胞均有典型的板层小体,反映肺组织某些晚期出现的细胞亚结构尚正常。结论膈疝早期胎鼠肺既已存在发育不良,而非晚期发育时所形成。提示膈疝肺发育不良的处理应在肺发育早期即行干预。
Objective To investigate the mechanism of congenital diaphragmatic hernia (CDH) pulmonary dysplasia and to study the ultrastructural features of CDH model fetal lung tissue at different developmental stages. Methods Seven Sprague-Dawley (SD) pregnant rats were randomly divided into two groups: diaphragmatic hernia group (n = 4): Nitrofen (125 mg / mouse, dissolved in 2 ml of olive oil) Rats in control group (n = 3) were given gavage with 2 ml of olive oil at 9.5 d of gestation One time, 10 fetuses were harvested respectively on 16 d, 18 d and 21 d of SD rats. Twenty-six days fetal rat lung tissue sections were observed by transmission electron microscopy; 18 d fetal rat lung tissue HE staining, transmission electron microscopy and statistics of the incidence of diaphragmatic hernia; 21 d fetal lung tissue in addition to HE staining, transmission electron microscopy , Statistics of the incidence of diaphragmatic hernia, calculate fetal lung weight to body weight ratio (Lw / Bw). Results Diaphragmatic hernia group fetal lung weight / body weight ratio was significantly lower than the control group (0.0238 vs.0.0430, P = 0.04); diaphragmatic hernia group 18 d and 21 d fetal diaphragmatic hernia incidence rates were 90.00% and 82.35%, respectively, Diaphragmatic hernia group showed fetal lung dysplasia, while the control group of fetal rats at 18 d and 21 d were no diaphragmatic hernia occurred; (2) Compared with the control group, diaphragmatic hernia group 16 d fetal lung ultrastructure also showed lung development Adverse changes: a wide substrate, content is very small; the main epithelial cells in the lung atrophy, ribosome abundance; bronchial microvilli; 18 d and 21 d of the sample observations show that with the extension of pregnancy, the above characteristics (3) In control group and diaphragmatic hernia group, typical lamellar bodies of fetal rat alveolar type II epithelial cells were found at 21 d of pregnancy, reflecting the normal subcellular structure of some advanced cells in lung tissue. Conclusion Diaphragmatic hernia early embryonic rat lung both dysplasia, rather than the late development of the formation. Tip Diaphragmatic hernia treatment of lung dysplasia should be in the early stages of lung development intervention.