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|本期目录/Table of Contents|

冠脉原位血栓大鼠血浆vWF水平的变化意义

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第3期
页码:
351-353,357
栏目:
基础研究
出版日期:
2009-05-15

文章信息/Info

Title:
Change and significance of vWF in a model of rat coronary thrombosis in situ
作者:
熊信林1; 谢建1; 王朝晖1; 王珏2
华中科技大学同济医学院：1.附属协和医院心血管疾病研究所，2.2004级7年制临床班，湖北 武汉，430022
Author(s):
XIONG Xin-lin1;  XIE Jian1;  WANG Zhao-hui1;  WANG Jue2
1.Institute of Cardiology, Union Hospital, 2.Class of 7-year program, undergraduate of 2004 grade, Tongji Medical College, Huazhong University of Science Technology, Wuhan 430022, Hubei, China
关键词:
冠状动脉; 原位血栓; 血管性假血友病因子; 月桂酸钠; 大鼠
Keywords:
coronary artery;  thrombus in situ;  von Willebrand factor;  sodium laurate;  rat
分类号:
R552
DOI:
-
文献标识码:
A
摘要:
目的 探讨冠脉原位血栓大鼠血浆血管性假血友病因子（vWF）水平的变化及意义。方法 将雄性SPF级SD大鼠78只，随机分为模型组（n=36）、假手术组（n=36）和正常对照组（n=6），模型组与假手术组按术后1 h，1，7，14，21，28 d各分6只。模型组经主动脉根部注入月桂酸钠，假手术组注入生理盐水，正常对照组不做任何处理。将心肌切片经HE与纤维素快速染色后，观察冠脉微血管原位血栓的形成。用ELISA检测血浆中vWF的水平。用超声心动图检查心脏的结构与功能。结果 模型组大鼠心肌微血管中，可见血小板纤维蛋白血栓，有原位血栓形成的微血管数量显著增加（P<0.01）；血浆中vWF的水平明显升高(P<0.05)；心脏扩大，心功能降低；而假手术组和正常对照组未见明显变化。 结论 冠脉微血管内皮细胞损伤释放的vWF可介导冠脉微血管内以血小板纤维蛋白沉积为主的原位血栓形成。
Abstract:
AIM To explore the changes and significance of plasma von Willebrand factor (vWF) levels in rat with coronary thrombosis in situ. METHODS Seventy-eight Sprague-Dawley male rats were randomly divided into model group (n=36), sham operation group (n=36) for different time (1 h, 1, 7, 14, 21, 28 d; n=6, respectively）and normal control group (n=6). After closing the aorta, sodium laurate was injected into the aortic root in model group, the rats in sham operation group were injected with physiologic saline, and the rats in normal group remained untreated. Microthrombs were detected with HE staining and modified Martius-Sarlet-Blue stains (MMSB), plasma vWF was measured by ELISA and cardiac structure and function were measured by echocardiogram. RESULS Many microthrombs were observed in the rat coronary microvasculature, vWF increased in plasma, the cardiac function decreased and the heart was enlarged in model group compared with those in sham operation group (P<0.05). No significant changes were observed in sham operation group and normal group. CONCLUSION The functional disorder of endothelial cells triggered by sodium laurate induces the increase of vWF in the coronary artery’s microvasculature and forms thrombosis with platelets and fibrin, which leads to the remodel of the heart.

参考文献/References

[1］ Skyschally A, Leineweber K, Gres P, et al. Coronary microembolization［J］. Basic Res Cardiol, 2006 , 101(5):373-382.

［2］ Ray KK, Morrow DA, Gibson CM, et al. Predictors of the rise in vWF after ST elevation myocardial infarction: implications for treatment strategies and clinical outcome: An ENTIRE-TIMI 23 substudy［J］. Eur Heart J, 2005, 26(5):440-446.

［3］ Chen Y, Ge JW, Deng BX. A new rat model of cerebral infarction based on the injury of vascular endothelial cell［J］. Chin J Integr Med, 2005, 11(3):195-200.

［4］ Olsen EH, McCain AS, Merricks EP, et al. Comparative response of plasma VWF in dogs to up-regulation of VWF mRNA by interleukin-11 versus Weibel-Palade body release by desmopressin (DDAVP)［J］. Blood, 2003, 102(2):436-441.

备注/Memo

备注/Memo:
收稿日期：2008-4-29.基金项目：国家重点基础研究发展计划（973计划）项目资助（2007CB512000，2007CB512005） 通讯作者：王朝晖，教授，博士，主要从事冠心病与微血栓研究Email:wwwzh@public.wh.hb.cn 作者简介：熊信林，医师，硕士Email：xinlin393@163.com
更新日期/Last Update: 2009-05-18