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目的对先天性食管闭锁患儿食管肌层进行电镜观察和免疫组化检测,研究其超微结构变化及神经递质表达的特点。方法食管闭锁组:2003年6月~2004年6月间新生儿先天性食管闭锁伴食管气管瘘远端食管肌层组织10例;对照组:非食管疾病死亡新生儿食管中段组织10例。分别进行HE染色光镜观察、透射电镜观察和NSE、SP、VIP和NOS的免疫组化检测。结果光镜下,食管闭锁组肌间神经丛分布稀疏,4.2±0.6/10×视野,神经节细胞减少,细胞核偏位,深染。电镜下,食管闭锁组平滑肌纤维线粒体肿胀,内质网扩张。线粒体细胞膜边缘现象明显。在肌间神经丛突触末梢中,核心小泡/清亮小泡较对照组明显增高(0.511±0.139vs0.192±0.020,P<0.05)。免疫组化染色食管闭锁肌间神经丛及神经节细胞的NSE,SP表达阳性率分别为20%和10%,明显低于对照组(90%和80%,P<0.05);VIP和NOS表达阳性率分别为90%和90%,明显高于对照组(30%和10%,P<0.05)。结论食管闭锁患儿食管肌层存在内源性神经结构缺陷和神经递质表达异常。
Objective To observe the changes of ultrastructure and the expression of neurotransmitter in esophageal muscle of children with congenital esophageal atresia by electron microscopy and immunohistochemistry. Methods Esophageal atresia group: 10 cases of congenital esophageal atresia with esophageal tracheal fistula distal esophageal muscle tissue from June 2003 to June 2004; control group: 10 cases of non-esophageal disease neonates died of middle esophageal tissue. Light microscopy, transmission electron microscopy and immunohistochemistry of NSE, SP, VIP and NOS were performed respectively. Results Under the light microscope, the myenteric plexus was sparsely distributed in the esophageal atresia group, 4.2 ± 0.6 / 10 × visual field, decreased ganglion cells, nuclear deviation and deep staining. Electron microscope, esophageal atresia smooth muscle fiber mitochondria swelling, endoplasmic reticulum dilatation. Mitochondrial membrane edge of the obvious phenomenon. In the myenteric plexus synaptic terminals, the number of core vesicles / clear vesicles was significantly higher than that of the control group (0.511 ± 0.139 vs 0.192 ± 0.020, P <0.05). The positive rates of NSE and SP expression in the myenteric plexus and ganglion cells in the esophageal atresia were 20% and 10%, respectively, which were significantly lower than those in the control group (90% and 80%, P <0.05) The positive rates were 90% and 90%, respectively, which were significantly higher than those in the control group (30% and 10%, P <0.05). Conclusion Esophageal atresia in children with esophageal muscle endogenous nerve structural defects and neurotransmitter expression abnormalities.