中文摘要：

在桅杆房间和动脉粥样硬化之间的关系的背景学习主要依赖于病理学的观察和细胞学实验。在匾和他们我们使用了的可能的机制上调查桅杆房间 degranulation 的效果被放了的 apolipoprotein E 猛烈老鼠 perivascular 有桅杆房间 degranulator 混合物 48-80 .Methods 的普通颈动脉领子四十只 apolipoprotein E 猛烈老鼠被喂一本西方类型的食谱并且恰好与 perivascular 的放置操作了普通颈动脉领子。在外科以后的四个星期，老鼠每隔一天 intraperitoneally 在 4 次与复合 48-80 (0.5 mg/kg ) 或 D 丝等被注射。tryptase 的浆液类脂化合物和活动被测量。织物节与 hematoxylin 和曙红被染色。相应的节对巨噬细胞特定的抗原，光滑的肌肉肌动朊， interleukin-1 和货车 Willebrand 因素与抗体与 toluidine 蓝色并且 immunohistochemically 被染色。同时，基本成纤维细胞生长因素被检测由在 situ 杂交和 immunofluorescence.Results，没有病理学的变化在普通颈动脉非领子放置被观察，但是在两个的普通颈动脉领子放置的 atherogenesis 组织。匾区域有重要增加((5.85 吗？

英文摘要：

Background Study of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80. Methods Forty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 （0.5 mg/kg） or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, a-smooth muscle actin, interleukin-1β and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence. Results No pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area （（5.85±0.75）×10^4 vs （0.86±0.28）×10^4 um^2, P 〈0.05）, the degree of lumen stenosis （（81±15）% vs （41±12）%, P 〈0.05）, the activity of tryptase in serum （（0.57±0.13） U/L vs （0.36±0.10） U/L, P 〈0.05）, and the percentage of degranulated mast cells （（80.6±17.8）% vs （13.5±4.1）%, P 〈0.05）. The expressions of macrophage-specific antigen, α-smooth muscle actin, interleukin-1β, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group. Conclusions Perivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque are