缺血-再灌注对冠脉内皮功能的影响及氧自由基的作用

Effects of ischemiareperfusion on coronary endothelial function and role of oxygen free radicals in this process in rats

目的：了解缺血－再灌注对冠脉内皮功能的影响及氧自由基的作用。方法：制备大鼠Ｌａｎｇｅｎ－ｄｏｒｆ灌注心脏，局部缺血３０ｍｉｎ后再灌注，观察内皮依赖舒张介质乙酰胆碱（Ａｃｈ）及内皮非依整舒张介质硝酸甘油（ＮＴＧ）对冠脉血管的作用，测定心肌超氧化物歧化酶（ＳＯＤ）及丙二醛（ＭＤＡ）样物质，在缺血期至再灌注１０ｍｉｎ，用重组人ＳＯＤ灌注心脏，了解Ａｃｈ、ＮＴＧ对冠脉血管作用的影响。结果：Ａｃｈ舒血管作用被逆转为缩血管效应，ＮＴＧ舒血管作用不受影响，ＳＯＤ明显降低，而ＭＤＡ明显升高，用重组人ＳＯＤ灌注心脏，Ａｃｈ舒血管作用可得以保护。结论：缺血－再灌注可损伤离体大鼠心脏冠脉内皮合成和释放内皮舒张因子（ＥＤＲＦ）的功能且氧自由基参与了这种损伤过程。

Objective: To study the effects of ischemiareperfusion on coronary endothelial function and role of oxygen free radicals in this process. Methods: The rat hearts were perfused with Langendorff method. After regional ischemia for 30 min, they were reperfused to the effects of acetylcholine (Ach), one of the endotheliumdependent vasodilators, and nitroglycerin (NTG), one of the endotheliumindependent vasodilators, on the coronary vessels and determine the contents of myocardial superoxide dismutase (SOD) and malondialdehyde (MDA). Following ischemia for another 30 min and reperfusion for 10min, the hearts were perfused with human recombinant SOD to observe its influence on the effects of Ach and NTG. Results: The vasodilation by Ach was reversed to the vasoconstriction while that by NTG was not influenced by ischemiareperfusion. The level of SOD was significantly reduced but that of MDA increased after reperfusion. Human recombinant SOD exerted protective effects on vasodilation by Ach when it was used at the beginning of ischemia. Conclusion: Coronary endothelial dysfunction can be caused by ischemiareperfusion and might be related to reduction or loss of the ability of endotheliumderived relaxing factor produced and released by coronary endothelium. Oxygen free radicals take part in endothelial damage during reperfusion and superoxide anionss is thought to play an important role in this process.