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近年来,黏附分子与炎性反应在经皮冠状动脉介入治疗术后再狭窄发生中的作用受到重视[1] ,已证实细胞间黏附分子1(ICAM 1)水平的增加与冠状动脉介入治疗术后的再狭窄显著相关[2 ,3 ] 。血管紧张素Ⅱ(AngⅡ)有强烈的致炎症作用,可刺激内皮细胞ICAM 1等黏附分子的表达[4] ,增加内?
In recent years, the role of adhesion molecules and inflammatory responses in the restenosis after percutaneous coronary intervention has been emphasized [1]. It has been demonstrated that the increase of intercellular adhesion molecule 1 (ICAM 1) level and coronary artery interventional therapy After restenosis was significantly correlated [2,3]. Angiotensin Ⅱ (Ang Ⅱ) has a strong role in inflammation, can stimulate endothelial ICAM 1 and other adhesion molecules [4], increased?