大鼠结核性胸膜炎模型和病理的研究

发布时间：2018-01-05 02:33

本文关键词：大鼠结核性胸膜炎模型和病理的研究　出处：《天津医科大学》2007年硕士论文　论文类型：学位论文

【摘要】：目的：探讨建立大鼠结核性胸膜炎模型的方法以及观察并初步研究大鼠结核性胸膜炎不同时段胸膜大体、光镜、电镜病理学改变。方法：健康Wistar大鼠30只,选取26只为实验组,4只为对照组。30只大鼠同时接种卡介苗(BCG)悬液O.1ml(0.06mg),5周后作胸腔穿刺术。实验组注入标准人型结核菌株H37Rv结核分枝杆菌悬液1m1(每毫升含菌量0.03mg),建立结核性胸膜炎大鼠模型。模型制作后第2、4、6、8、10、12、14、16、18、22、30天分批处死大鼠,每次2只。对照组,注入生理盐水lml,注入后第2、4天处死大鼠,每次2只。观察不同时段胸膜大体、光镜、电镜病理学改变。结果：30只大鼠试验组26只成功复制出结核性胸膜炎模型,对照组4只未出现结核性胸膜炎表现。病理学观察病变早期,胸腔积液量逐渐增多,第6-8天达到高峰,以后胸水逐渐减少,第16-22天,胸水基本消失。胸膜早期充血、水肿、纤维蛋白渗出,胸膜下淋巴细胞浸润,在淋巴细胞团间可见上皮样细胞,胸膜有灶性坏死灶,可见肉芽肿结节,有间皮细胞逐渐破损的表现；后期胸膜肥厚、粘连,可见结核结节、糜烂灶,光镜下上皮样细胞团增多,可见纤维组织增生,干酪样坏死,电镜下间皮细胞细胞膜、细胞质大部分缺损,可见成纤维细胞及纤维细胞,间皮细胞下结缔组织增生,有大量胶原纤维,呈束状,排列不规则。结论： 1、接种卡介苗5周后向大鼠胸腔注入标准人型结核菌株H37RV结核分枝杆菌悬液可以建立结核性胸膜炎的动物模型,胸膜病理观察符合结核性胸膜炎的特征,坏死组织抗酸染色发现抗酸杆菌。 2、结核性胸膜炎病理改变：早期以渗出为主,炎细胞浸润,间皮细胞、细胞器不同程度破坏,继之间皮细胞基本破坏消失,胶原纤维增生,巨噬细胞转化为上皮样细胞、Langhans巨细胞,形成结核结节,或出现干酪样坏死,三种病理改变可同时存在。
[Abstract]:Objective: to explore the method of establishing the model of tuberculous pleurisy in rats and to observe and study the pathological changes of the pleura of rats with tuberculous pleurisy in different periods. Methods: 30 healthy Wistar rats were inoculated with 0.1 ml BCG suspension (0. 06mg), and 26 rats were selected as experimental group (4 rats as control group). 30 rats were inoculated with BCG suspension at the same time. After 5 weeks, thoracic puncture was performed. The standard human tuberculous strain H37Rv was injected into the experimental group with a suspension of 1 ml of Mycobacterium tuberculosis (0.03mg per milliliter). The rat model of tuberculous pleurisy was established. After the model was made, the rats were killed in batches for 30 days with 2 rats in control group. The rats were killed on the 2nd day after the injection of normal saline, 2 rats were killed each time. The pathological changes of the pleura were observed under light microscope and electron microscope at different time periods. Results the tuberculous pleurisy model was successfully made in the experimental group of 30% rats and the tuberculous pleurisy was found in 4 rats in the control group. The amount of pleural effusion increased gradually in the early stage of pathological observation. The pleural effusion reached its peak on the 6th to 8th day, and then decreased gradually. On the 16-22 days, the pleural effusion disappeared basically. The pleural effusion was hyperemia, edema, fibrin exudation and subpleural lymphocytic infiltration in the early stage. Epithelioid cells could be seen between lymphocyte clusters, focal necrotic foci in pleura, granulomatous nodules, and gradually damaged mesothelial cells. Late pleural hypertrophy, adhesion, tuberculous nodules, erosion focus, light microscope epithelioid cell mass increased, visible fibrous tissue proliferation, caseous necrosis, electron microscopic mesothelial cell membrane, most of the defects of the cytoplasm. Fibroblasts and fibroblasts, connective tissue proliferation under mesothelial cells, a large number of collagen fibers, bundles, irregular arrangement. Conclusion: 1. The animal model of tuberculous pleurisy could be established by injecting standard human tuberculosis strain H37RV Mycobacterium tuberculosis suspension into the thoracic cavity of rats after 5 weeks of BCG inoculation. Pleural pathological observation was consistent with the characteristics of tuberculous pleurisy. Acid-fast bacillus was found in necrotic tissue. 2, pathological changes of tuberculous pleurisy: early stage was mainly exudate, inflammatory cells infiltrated, mesothelial cells and organelles destroyed to varying degrees, then the basic destruction of skin cells disappeared and collagen fiber proliferated. Macrophages were transformed into epithelioid Langhans giant cells to form tuberculous nodules or casein necrosis.
【学位授予单位】：天津医科大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R521.7;R-332

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