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目的研究噪声性内耳损伤过程中耳蜗微循环的病理变化以及内皮素(endothelin,ET)在这一病理过程中的作用及意义。方法30只大鼠按电脑产生随机数字法分为5组:对照组、噪声暴露(115dB白噪声每天8h)1、4、8和15d组。分别用扫描电镜观察毛细胞的形态,血管纹铺片观察耳蜗微循环的状态,放射免疫方法检测血浆ET含量,免疫组化染色观察ET1、ETA、ETB的分布。结果噪声4、8、15d组出现了血管纹明显缺血,外毛细胞形态异常。血浆ET于4d组出现暂时性升高。ET1于耳蜗组织中有广泛的阳性表达,噪声暴露前后差异无统计学意义;ETA主要分布于血管纹中间细胞与微血管壁周围的细胞,对照组与1d组表达呈弱阳性(+),噪声4、8、15d组表达呈强阳性(+++)。ETB主要分布于血管纹毛细血管内皮细胞,其变化趋势与ETA相似。结论噪声性内耳损伤过程中出现了明显的耳蜗微循环障碍,同时大鼠耳蜗组织的ET系统活性增高,二者在时间上有明显的一致性。推测噪声所致的耳蜗微循环障碍过程中ET起了重要的介导作用。
Objective To investigate the pathological changes of cochlear microcirculation and the role and significance of endothelin (ET) in this pathological process. Methods Thirty rats were randomly divided into five groups according to the random number generated by computer: control group, noise exposure (115dB white noise 8h everyday) for 1, 4, 8 and 15 days. The morphology of hair cells was observed with scanning electron microscope (SEM). The microcirculation of cochlea was observed with vascularized smears. The content of plasma ET was detected by radioimmunoassay. The distributions of ET1, ETA and ETB were observed by immunohistochemistry. Results In the 4, 8 and 15 d groups, there was obvious ischemic vascular pattern and abnormal morphology of the outer hair cells. Plasma ET increased temporarily in 4d group. ET1 was widely expressed in cochlea tissues, and there was no significant difference before and after noise exposure. ETA mainly distributed in the middle of vascular pattern and cells around the microvascular wall. The expression of ET1 was weak positive (+) and noise 4 , 8,15d group was strongly positive (+++). ETB is mainly distributed in vascular capillary endothelial cells, the trend of which is similar to that of ETA. Conclusions There is obvious disturbance of cochlear microcirculation in the process of noise-induced inner ear injury. At the same time, the activity of ET system in rat cochlea is increased. There is a clear consistency in time between the two. It is speculated that noise plays an important mediating role in the process of cochlear microcirculation disturbance.