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目的 建立大鼠多发性大动脉炎模型，并探讨其发病机制。方法 １０周龄雌性ＳＤ大鼠４０只，随要分为４组：１个对照组（ＮＳ）和３个实验组。对照组每天给予生理盐水２ｍｌ灌胃，实验组分别给予己烯雌酚１ｍｇ／（ｋｇ·ｄ）（ＤＥＳ１组）、２ｍｇ／（ｋｇ·ｄ）（ＤＥＳ２组）和２ｍｇ／（ｋｇ·ｄ）加三苯氧胺１ｍｇ／（ｋｇ·ｄ）（ＴＡＭ组）胃饲３个月后，观察病理和超微结构改变。结果 病变动脉呈灰白色，管壁僵硬，与无明显病变动脉交替出现；光镜下平滑肌细胞聚集成团束状，晚期被大量纤维组织所取代；电镜下变性平滑肌细胞核膜模糊或消失，内质网扩张，线粒体肿胀，在增生的平滑肌细胞周围有许多胶原纤维，病变晚期大量胶原纤维中夹杂萎缩的平滑肌细胞。ＤＥＳ１组、ＴＡＭ组和对照组未发现明显异常。结论 本实验以雌激素诱发大鼠产生类似于人类多发性大动脉炎的疾病模型，提示雌激素参与本病的发生发展过程。
Objective To establish a rat model of multiple arteritis and to explore its pathogenesis. Methods Forty female 10-week-old female Sprague-Dawley rats were randomly divided into 4 groups: one control group (NS) and three experimental groups. The rats in the control group were administered with 2 ml of saline every day. The rats in the experimental group were given diethylstilbestrol 1 mg / (kg · d) (DES1), 2 mg / (kg · d) (DES2) and 2 mg / (kg · d) (Kg · d) (TAM group) for 3 months after gastric feeding, observe the pathological and ultrastructural changes. Results The diseased arteries were gray-white and the walls were rigid and alternated with no obvious diseased arteries. The smooth muscle cells clustered into clusters under the light microscope and replaced by a large number of fibrous tissues in the late stage. The nuclear membrane of the degenerative smooth muscle cells was vague or disappeared under electron microscope, Expansion, mitochondria swelling, hyperplasia of smooth muscle cells in the surrounding many collagen fibers, late lesions of a large number of collagen fibers in the atrophy of smooth muscle cells. No significant abnormalities were found in DES1 group, TAM group and control group. Conclusion In this study, estrogen-induced rat models of human polyarteritisemia were established, suggesting that estrogen participates in the pathogenesis of this disease.