PCI术后心肌缺血损伤机制与治疗的研究进展  

The Research Progress of Mechanism and Treatment of Myocardial Ischemia/Reperfusion Injury after PCI

作　　者：付艳东[1] 赵翠萍[1] 

机构地区：[1]哈尔滨医科大学附属第一医院心血管内科,黑龙江哈尔滨150000

出　　处：《现代生物医学进展》2012年第35期6992-6994,6968,共4页Progress in Modern Biomedicine

摘　　要：经皮冠状动脉介入治疗术(percutaneous coronary artery intervention,PCI术)是冠心病患者血运重建的重要手段,但临床观察显示PCI术后经出现慢血流、无复流,再灌注心律失常及心肌酶学的升高,直接影响患者的预后。因此,减少PCI术后的心肌损伤是改善冠心病患者经PCI术后预后的关键。目前研究认为PCI术后心肌缺血再灌注损伤的发病机制主要与心肌再灌注时与氧自由基生成增多、细胞内Ca2+超载、心肌细胞能量代谢障碍、微血管损伤、粒细胞浸润以及心肌细胞的凋亡等多方面的作用有关,而PCI术后心肌损伤的保护治疗方面主要有药物与器械两方面。本文就PCI术后心肌缺血再灌注损伤的机制及保护治疗的研究进展作一综述。PCI is an important way of revascularization in coronary heart disease patients,but clinical observation show that slow flow,no-refiow,reperfusion arrhythmia,and the rise of myocardial enzymes are often found in PCI postoperative.Therefore,how to reduce the myocardial injury is the crucial research content.At present,there are many assumptions and reports about the pathogenesis of myocardial ischemia reperfusion injury,the main and relevant role is that the increased formation with oxygen free radicals,cellular Ca2＋ overload,microvessel damage,and granulocytic infiltration and myocardial cell apoptosis,et al.In this paper,mechanism and protection treatment of myocardial ischemia reperfusion in PCI postoperative are summarized.

关 键 词：心肌缺血 再灌注损伤 氧自由基 细胞凋亡 缺血预适应 

分 类 号：R541.4[医药卫生—心血管疾病]