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|本期目录/Table of Contents|

血管外膜损伤后血管内皮的功能及形态变化

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第3期
页码:
347-350
栏目:
基础研究
出版日期:
2009-05-15

文章信息/Info

Title:
Changes of vascular endothelium in function and morphology after adventitial injury
作者:
汤月霞1; 2; 梁春1; 吴宗贵1
1.上海长征医院心内科，上海 200003;2.济南军区青岛第一疗养院，山东 青岛 266071
Author(s):
TANG Yue-xia1; 2;  LIANG Chun1;  WU Zong-gui1
1.Department of Cardiology, Changzheng Hospital, Shanghai 200003, China; 2.Qingdao First Sanatorium, Jinan Military Area Command, Qingdao 266071, Shandong, China
关键词:
血管外膜损伤; 内膜增生性病变; 内皮依赖性舒张功能; 兔
Keywords:
adventitial injury;  intimal hyperplasia lesion;  endothelial-dependent vasorelaxation function;  rabbit
分类号:
R543.5
DOI:
-
文献标识码:
A
摘要:
目的 探讨血管内皮损伤在外膜损伤致内膜病变中的作用。方法 选用纯种新西兰大白兔，采用胶原酶消化＋机械分离的方法建立外膜损伤动物模型，HE染色后，观察外膜损伤血管的形态变化。采用Medlab-U/4C501生物信号采集处理系统检测血管内皮依赖性舒张功能，电镜下观察血管内皮细胞的微观形态变化。用实时PCR检测单核细胞趋化蛋白-1（MCP-1）mRNA的表达。结果 外膜损伤后3 d血管内皮依赖性舒张功能减退及内皮细胞损伤，7 d出现内膜增生性病变。结论 血管外膜损伤可能通过损伤血管内皮导致内膜病变的形成。
Abstract:
AIM To explore the role of vascular endothelial injury in the intimal lesion caused by adventitial injury. METHODS Models of New Zealand rabbits with vascular adventitial injury were established by collogenase digestion and mechanical dissection. HE staining was used to detect the morphological changes in vessels after adventitial injury. Endothelial-dependent vasorelaxation function was detected with Medlab-U/4C501 biological signal collection and analysis system. Morphological changes in endothelial cells were observed under electron microscope and real-time PCR were used to determine the expression of monocyte chemotactic protein-1（MCP-1) mRNA. RESULTS Compared with that in control vessels, the endothelial-dependent vasorelaxation function was failing and endothelial cell injuries were found 3 days after injury. Expression of MCP-1 mRNA increased 3 days after injury and intimal hyperplasia was observed 7 days after injury. CONCLUSION Vascular adventitial injury may cause vascular endothelial injury and then lead to intimal lesion.

参考文献/References

[1］ Prescott MF, McBride CK, Court M. Development of intimal lesions after leukocyte migration into the vascular wall［J］. Am J Pathol, 1989, 135(5):835-846.

［2］ Barker SG, Tilling LC, Miller GC, et al. The adventitia and atherogenesis: removal initiates intimal proliferation in the rabbit which regresses on generation of a ‘neoadventitia’［J］. Atherosclerosis, 1994,105(2):131-144.

［3］ 汤月霞，刘永，王华，等. 血管外膜剥离致内膜增生病变的动物模型［J］. 中国动脉硬化杂志， 2008， 16（1）：65-68.

［4］ Sartore S, Chiavegato A, Faggin E, et al. Contribution of adventitialfibroblast s to neointima formation and vascular remodeling: from innocent bystander to active participant［J］. Circ Res, 2001, 89(12):1111-1121.

［5］ Shi Y, Niculescu R , Wang D , et al. Increased NAD(P) H oxidase and reactive oxygen species in coronary arteries after balloon injury［J］. Arterioscler Thromb Vasc Biol, 2001, 21(5):739-745.

［6］ Siow RC, Mallawaarachchi CM, Weissberg PL, et al. Migration of adventitial myofibroblasts following vascular balloon injury: insights from in vivo gene transfer to rat carotid arteries［J］. Cardiovasc Res, 2003, 59(1):212-221.

［7］ Allbutt TC. Diseases of the artries including angina pectoris［M］. London: Macmillan Co, 1915:468.

［8］ Schwartz CJ, Mitchell JR. Cellular infiltration of the human arterial adventitia associated with atheromatous plques［J］. Circulation, 1962, 26(1):73-78.

［9］ Higuchi ML, Gutierrez PS, Bezerra HG, et al. Comparison between adventitial and intimal inflammation of ruptured and nonruptured atherosclerotic plaques in human coronary arteries［J］. Arq Bras Cardiol, 2002, 79(1):20-24.

［10］Rayner K, Van Eersel S, Groot PH, et al. Localisation of mRNA for JEPMCP21 and its receptor CCR2 in atherosclerotic lesions of the Apo E knockout mouse［J］. J Vasc Res, 2000, 37(2):93-102.

［11］牟华明，王利娟，闫振成，等. 血管外膜介导的炎症反应对血管平滑肌细胞增殖的影响［J］. 解放军医学杂志, 2007, 7(7):734-737.

［12］Hu Y, Zhang Z, Torsney E, et al. Abundant progenitor cells in the adventitia contribute to atherosclerosis of vein grafts in ApoE-deficient mice［J］. J Clin Invest, 2004, 113(9):1258-1265.

［13］Cai H, Harrison DG. Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress［J］. Circ Res, 2000, 87(10):840-844.

［14］Hordijk PL. Endothelial signalling events during leukocyte transmigration［J］. FEBS J, 2006, 273(19):4408-4415.

［15］Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk［J］. Arterioscler Thromb Vasc Biol, 2003, 23(2):168-175.

［16］Katz SD, Hryniewicz K, Hriljac I, et al. Vascular endothelial dysfunction and mortality risk in patients with chronic heart failure［J］. Circulation, 2005, 111(3):310-314.

备注/Memo

备注/Memo:
收稿日期：2008-3-13.通讯作者：吴宗贵，教授，主要从事动脉粥样硬化发病机制的研究Email：zgwu@medmail.com.cn 作者简介：汤月霞，主治医师，博士Email：penglaitang@163.com
更新日期/Last Update: 2009-05-18