CAJ | 학술논문

近年来，我国急性心肌梗死发病率明显上升，已接近国际平均水平。心肌缺血／再灌注损伤（ I／RI）是缺血心肌恢复血运后的常见并发症。研究表明，I／RI与线粒体功能结构损害关系密切。心肌发生缺血／再灌注时，心肌细胞发生一系列病理生理变化。迄今为止，已发现多种手段可用来减弱I／RI，该保护通路包括乙酰胆碱、一氧化氮合酶、一氧化氮、内皮细胞、蛋白激酶 Cε、线粒体连接蛋白43、线粒体ATP敏感性钾离子通道。
근년래，아국급성심기경사발병솔명현상승，이접근국제평균수평。심기결혈／재관주손상（ I／RI）시결혈심기회복혈운후적상견병발증。연구표명，I／RI여선립체공능결구손해관계밀절。심기발생결혈／재관주시，심기세포발생일계렬병리생리변화。흘금위지，이발현다충수단가용래감약I／RI，해보호통로포괄을선담감、일양화담합매、일양화담、내피세포、단백격매 Cε、선립체련접단백43、선립체ATP민감성갑리자통도。
The incidence of acute myocardial infarction has been ascending notably in recent years and is reaching international average.Myocardial ischemia/reperfusion injury(I/RI) is a common complication after recover of the blood supply in ischemic myocardium.Studies show that I/RI is closely associated with impairment of mitochondrial function and structure .Cardiomyocytes suffer from a series of pathophysiological changes when ischemia/reperfusion occurs in myocardial infarction.So far multiple measures have been dis-covered to attenuate I/RI.This protective pathway includes acetylcholine,nitrogen monoxide synthase,nitro-gen monoxide, protein kinase Cε, mitochondrial connexin 43 and mitochondrial ATP sensitive potassium channel.