鼻-鼻窦炎致嗅觉功能障碍大鼠模型的建立

Studies of a Rat Model of Dysosmia Caused by Rhino-sinusitis

目的通过鼻-鼻窦炎导致嗅觉功能障碍的大鼠模型的建立，探讨嗅觉功能障碍与鼻-鼻窦炎病理变化程度及黏膜上皮厚度之间的关系。方法采用鼻腔接种肺炎链球菌法制作鼻-鼻窦炎大鼠模型，埋藏食物小球法（buried food pellet，BFP）测试大鼠的嗅觉功能。实验过程持续4周，每周处死一批动物，收集鼻腔-鼻窦黏膜标本，HE染色法观察鼻腔-鼻窦黏膜炎症反应程度及黏膜上皮层厚度的变化并探讨这类病理改变与嗅觉功能障碍的关系。结果模型组大鼠鼻腔-鼻窦黏膜均有不同程度的炎症反应及黏膜上皮层变薄倾向，尤以造模后2周最为严重，至第4周时最轻。模型组大鼠嗅觉功能均比对照组减退，差异有统计学意义（P〈0．01），尤以造模后2周嗅觉功能最差，至第4周时相对改善。嗅觉功能变化与局部黏膜病理改变及黏膜上皮层厚度变化趋势相一致。结论鼻腔接种肺炎链球菌法可以在大鼠成功制作嗅觉功能障碍模型；模型动物的嗅觉功能障碍程度与其鼻腔-鼻窦黏膜炎症病理轻重及上皮层厚度存在正相关性。

Objective To investigate the association of dysosmia with the severe degree of inflammatory pathology and epithelial lamina thickness of nasosinuous mucosa among rats with experimental rhino-sinusitis through the establishment of model with dysosmia induced by such a lesion in an experimental study. Methods The model of dysosmia was established among rats by the use of Streptococcus pneumonia inoculated into nasal cavity to induce rhino-sinusitis at first, and then, to cause dysosmia in turn among the animals. Determination of olfactory function was carried out via the procedures of buried food pellet （BFP） among these modeling rats following rhino-sinusitis prepared successfully. The whole experimental course was lasted for 4 weeks, and all the rats were put into death at 4 intervals, one week at each interval. Followed were the procedures taken to collect naso-sinuous mucosal samples from these animals to determine the severe degree of inflammatory pathology and the thickness of epithelial lamina in naso-sinuous mucosa by HE staining program and to explore the association of pathological changes in naso-sinuous mucosa with the level of dysosmia based on an careful analysis on these experimental data. Results Various degrees of inflammatory pathology could be determined in the tissue samples ofnaso- sinuous mucosa among all the rats in modeling group, with a tendency to become thinner in the thickness of epithelial lamina during the pathology developing course. This kind of pathology was most marked at the 2 week and it gradually developed into the stage showing the lesion being the feeblest at the 4 week following the beginning of modeling. Followed was the damaged olfactory function among the modeling rats with significantly statistical implications （P〈0.01） when compared with that of controlling group, also most obvious at the 2 week and developed into the most feeble stage at the 4 week during the experimental course. There was a significant correlation of the changes in olfactory function with the severe degree of inflammatory pathology and epithelial lamina thickness in these naso-sinuous mucosa among these rats with such a lesion. Conclusions Dysosmia model can be successfully developed by the procedures inoculating Streptococcus pneumonia into nasal cavity of rats to induce rhino-sinusitis, and the damaged level of olfactory function of the modeling animals is positively correlated with the degree of inflammatory pathology in naso-sinuous mucosa and the thickness of epithelial lamina on it.