小鼠颈动脉狭窄模型与T细胞免疫缺陷的初步研究  被引量:2

Preliminary Study on Relationship between Restenosis in the Carotid Artery of a New Type Animal Model(BALB/c-nude Strain Mice) and Immunodeficiency of T Cells

在线阅读下载全文

作  者:穆军升[1] 朱洪生[1] 郑家豪[1] 山朝晖[1] 

机构地区:[1]上海第二医科大学附属仁济医院胸心外科,上海200001

出  处:《中国实验动物学杂志》2002年第1期5-7,共3页Chinese Journal of Laboratory Animal Science

摘  要:目的 建立一种血管再狭窄模型 ,排除T淋巴细胞的免疫排斥反应 ,更好地进行血管狭窄机制研究。方法 新近建立了一种新型BALB c nude裸鼠的颈动脉再狭窄模型 ,对其左颈总动脉进行了结扎 ,在 2周后作病理学观察。结果 BALB c nude在手术后 2周有明显的血管狭窄 ,并且结扎的动脉和周围组织粘连较轻 ;同时另一品系C57BL 6J小鼠在手术后 4周才出现明显的血管狭窄 ,而且动脉和周围组织粘连严重。结论 血管再狭窄是血管再构和新内膜形成的共同原因 ,在动脉狭窄模型的建立上BALB c nude较C57BLObjective Restenosis is one of the major cardiovascular illness.It can be assumed as a combination of neointima formation and arterial remodeling in response to injury.Methods We recently established a new type model in BALB/c-nude mice,after ligation of the left common carotid artery just proximal to the bifurcation resulting in 90% reduction of lumen area by a combination of intimal hyperplasia together with decreased diameter.In this study,neointima formation in C 57BL/6J mice and BALB/c-nude mice was compared.Results At two and four different weeks after the ligation,leukocyte infiltration was observed in the developing neointima,about a 90% reduction of luminal area was observed in C 57BL/6J four weeks after the ligation with severe adhesion between artery and tissue;while about a 90% reduction of luminal area was observed in BALB/c-nude only two weeks after the ligation with slight adhesion between artery and tissue was observed.Conclusion Vascular remodeling with neointima formation was the cause of restenosis,presumably by mediating leukocyte recruitment and the interaction between platelets and leukocytes,model of BALB/c-nude being better than that of C 57BL/6J.

关 键 词:小鼠 血管再狭窄 内皮 血管 移植免疫学 颈动脉狭窄模型 T细胞免疫缺陷 

分 类 号:R654.3[医药卫生—外科学] R543[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象