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冠状动脉狭窄与扩张患者的血浆NO、ET-1、MMP-9及TIMP-1水平变化 被引量:4

Alteration of NO,ET-1,MMP-9 and TIMP-1 plasma levels in coronary artery stenosis and ectasia
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摘要 目的探讨一氧化氮(NO)、内皮素-1(ET-1)、基质金属蛋白酶-9(MMP-9)和组织基质金属蛋白酶抑制物-1(TIMP-1)在冠状动脉损伤中可能的参与机制。方法选择我院行冠脉造影的患者,分为冠脉扩张组25例(单纯冠脉扩张7例;冠脉扩张合并少量斑块18例),冠脉粥样硬化组38例,冠脉正常组32例(冠脉完全正常14例;冠脉有少量斑块18例)。用ELISA法检测血浆NO、ET-1、MMP-9及TIMP-1水平。结果NO、NO/ET-1、MMP-9、MMP-9/TIMP-1在冠脉扩张、粥样硬化及正常组间存在显著差异(P<0.05)。进一步分亚组分析,单纯冠脉扩张组NO水平达到最高分泌峰值[(168±121)μmol/L],冠脉扩张合并少量斑块组MMP-9水平达到分泌最高值[(1977±1090)ng/L],ET-1和TIMP-1水平并没有统计学差异。结论冠脉扩张可能是抵抗动脉粥样硬化发生而启动的机体正常代偿功能,而冠状动脉粥样硬化是机体失去正常代偿功能所导致的血管损伤。 Objective To explore the mechanisms responsible for different coronary artery lesions with involvement of nitric oxide (NO), endothelin-1 (ET-1), matrix metalloproteinases-9 (MMP-9) and the matrix metalloproteinase inhibitor-1 ( TIMP-1 ). Methods The cases undergone coronary anography were collected and divided into three groups: group A,30 patients with the coronary artery ectasia(7 cases of simple coronary artery ectasia; 18 cases of the coronary artery ectasia coexisting a small amount of plaque) ;group B ,38 patients with coronary atherosclerosis; group C ,32 patients with with normal angiograph (14 cases of coronary artery completely normal; 18 cases with a small amount of coronary plaque only). Plasma NO, ET-1, MMP-9 and TIMP-1 level were measured by ELISA method. Results There are significant differences among three groups on NO level, MMP-9 levels, NO/ET-1 and MMP-9/TIMP-1(P〈0.05). Further sub-group analysis, NO advanced to peak value in isolated coronary eetasia, while MMP-9 rose to highest value in the coronary artery ectasia coexisting a small amount of plaque. Conclusion The coronary ectasia may be a compensatory mechanism to resist coronary artery atherosclerosis, while eoronary atherosclerosis is the result of reduced compensatory function.
出处 《基础医学与临床》 CSCD 北大核心 2009年第10期1031-1034,共4页 Basic and Clinical Medicine
基金 国家自然科学基金(30470726)
关键词 冠状动脉扩张 冠状动脉粥样硬化 冠状动脉狭窄 coronary artery ectasia coronary atherosclerosis coronary stenosis
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参考文献10

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同被引文献28

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