心肌缺血再灌注损伤的主要机制与相关药物治疗的研究进展  

Research on main mechanisms of MIRI and related drug therapy

作　　者：徐盟[1] 

机构地区：[1]中国医科大学

出　　处：《实用药物与临床》2014年第8期1052-1056,共5页Practical Pharmacy and Clinical Remedies

摘　　要：缺血性心肌病在治疗后可能发生缺血再灌注损伤,受损心肌的损伤程度加重,梗死面积扩大,这种现象的发生与多种机制有关,包括:钙超载、氧自由基增多、炎症反应等。随着心肌缺血的治疗技术的提高,缺血再灌注时期的治疗已成为缺血性心肌病的治疗重点,因此,针对防治该时期的药物研发也已成为重点。常见药物作用机制包括:减轻钙超载、抗炎症反应、抗氧自由基和改善能量代谢等。本文旨在对MIRI不同病理机制和相关药物的研究进展进行阐述。Ischemia-reprefusion injury （IRI）often occurred after ischemia myocardial is treated. When IRI occurred, the damaging degree of myocardial aggravated and infarction area expanded. The phenomenon is associated with a variety of mechanisms, including ： overloading calcium, increased oxygen free radicals, inflammation, etc. With the improvement of MIRI＇ s treating technology, treatments during MIRI become a key to treat ischemia myocardial. So re search of drugs for preventing or treating disease during MIRI has become the key point. Common mechanisms of drugs include：reducing calcium overloaded, anti-inflammation, resisting oxygen free radicals and improving energy meatabolism, etc. This article aims to summarize different pathologic mechanisms of MIRI and recent research of related drugs.

关 键 词：心肌缺血再灌注损伤(MIRI) 钠离子/钙离子交换蛋白 氧自由基 炎症因子 

分 类 号：R542.2[医药卫生—心血管疾病]