RELATIONSHIP BETWEEN INSUFFICIENCY OF TRNSMUCOSAL GAS EXCHANGE AND REFRACTORINESS OF MIDDLE EAR INFLAMMATORY DISEASE-EXPERIMENTAL AND CLINICAL STUDY.

粘膜间气体交换不足与中耳炎症性疾病难治性之间的关系-实验和临床研究。

基本信息

批准号：
09671762
负责人：
AOKI Kazuhiro
金额：
$ 1.86万
依托单位：
THE JIKEI UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

项目摘要

Mucosal lesion in the middle ear pneumatic space is closely related to the suppression of pneumatization. A transmucosal gas exchange function is clearly present in the mucosal epithelium of the middle ear pneumatic space. In persistent middle ear inflammation as represented by OME, the subepithelial layer of the middle ear mucosa is damaged, and the gas exchange function, mainly of diffusion of COィイD22ィエD2, is suppressed. Change in the TP in the middle ear cavity observed in patients with indwelt tube is also thought to be related to this gas exchange function ; the peak value of the TP had was lower in patients with severer mucosal lesion. In these patients, the peak value of the TP had increased after 18 or more months of tube indwelling, when the mucosa of middle ear cavity seemed to be recovered normal thin mucosa. This mucosal normalization was especially important in subepithelium because of thin layer with many capillary networks. This subepithelial mucosal normalizaiton was also confirmed by the repneumatization of the mastoid cell after two years of treatment. Therefore, it is assumed that the intractability of OME with suppressed mastoid cells is affected by the insufficiency of transmucosal gas exchange function, so the transmucosal gas exchange is involved in the on set and healing process of middle ear mucosal disease when it seems likely that normalization of transmucosal gas exchange function follows resolution of middle ear inflammation and the subsequent mucosal inflammation, and it is possible to estimate the severity of mucosal lesion by measuring the peak value of the TP.

在以OME为代表的持续性中耳炎症中，中耳充气间隙的粘膜病变与气化的抑制密切相关。中耳粘膜受损，气体交换功能（主要是COD22的扩散）受到抑制，中耳TP发生变化。留置管患者的耳腔观察也被认为与这种气体交换功能有关；在粘膜病变较严重的患者中，TP的峰值较低，18岁后TP的峰值有所增加。管留置数月或更长时间，此时中耳腔粘膜似乎恢复正常的薄粘膜，这种粘膜正常化在上皮下层尤其重要，因为薄层有许多毛细血管网络。治疗两年后，乳突细胞的重新气化也证实了上皮下粘膜的正常化。因此，推测乳突细胞受到抑制的OME的难治性受到跨粘膜气体交换功能不足的影响，因此跨粘膜气体交换受到影响。当中耳消退后跨粘膜气体交换功能似乎可能正常化时，参与中耳粘膜疾病的发病和愈合过程炎症反应及随后的粘膜炎症，通过测量TP的峰值可以估计粘膜病变的严重程度。