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实验性中耳炎中耳血管渗漏部位的识别与表征

Identification and characterization of middle ear vascular leakage sites in experimental otitis media.

作者信息

Goldie P, Hellström S

机构信息

Department of Anatomy, University of Umeá, Sweden.

出版信息

Ann Otol Rhinol Laryngol. 1990 Oct;99(10 Pt 1):810-6. doi: 10.1177/000348949009901011.

DOI:10.1177/000348949009901011
PMID:1699467
Abstract

The site of leakage in middle ear vessels was determined and characterized in experimental otitis media in rats. Middle ear effusion was induced by intravenous administration or local application in the tympanic bulla of substance P (SP), acetylcholine, and histamine. In another experiment, a 14 degrees C airstream was blown into the external auditory canal. Colloidal carbon was used to trace leakage sites at the light and electron microscopic levels. All mediators tested and the 14 degrees C airstream resulted in an increased number of leaking vessels in the pars flaccida and the middle ear mucosa. The leakage sites were restricted to capillaries and postcapillary venules. Increased numbers of degranulated pars flaccida mast cells were observed for SP only. Interendothelial gaps formed in leakage vessels after administration of mediators and stimulation of the external auditory canal with a 14 degrees C airstream. Also, cytoplasmic vesicle-like structures within the endothelial cells increased in number following SP and histamine treatment, suggesting that an increased permeability in experimental otitis media does not occur exclusively through interendothelial gaps.

摘要

在大鼠实验性中耳炎模型中,对中耳血管渗漏部位进行了定位和特征分析。通过静脉注射或在鼓泡局部应用P物质(SP)、乙酰胆碱和组胺来诱导中耳积液。在另一项实验中,将14℃的气流吹入外耳道。使用胶体碳在光镜和电镜水平追踪渗漏部位。所有测试的介质以及14℃的气流均导致松弛部和中耳黏膜渗漏血管数量增加。渗漏部位局限于毛细血管和毛细血管后微静脉。仅在SP作用后观察到松弛部脱颗粒肥大细胞数量增加。在给予介质和用14℃气流刺激外耳道后,渗漏血管中形成了内皮细胞间隙。此外,在SP和组胺处理后,内皮细胞内的细胞质囊泡样结构数量增加,这表明实验性中耳炎中通透性增加并非仅通过内皮细胞间隙发生。

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Identification and characterization of middle ear vascular leakage sites in experimental otitis media.实验性中耳炎中耳血管渗漏部位的识别与表征
Ann Otol Rhinol Laryngol. 1990 Oct;99(10 Pt 1):810-6. doi: 10.1177/000348949009901011.
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