缺血后适应减轻家兔急性心肌缺血/再灌注损伤的作用研究
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2009年第5期
- 页码:
- 643-647
- 栏目:
- 基础研究
- 出版日期:
- 2009-07-14
文章信息/Info
- Title:
- Abatement effect of myocardial injury by ischemic postconditioning during acute ischemia/reperfusion in rabbits
- Author(s):
- WANG Ling; LIN Rong; WU Bing; HONG Mei-man
- Department of Cardiovascular Diseases, Quanzhou First Hospital, Fujian Medical University, Quanzhou 362000, Fujian, China
- Keywords:
- myocardial infarction; ischemia/reperfusion injury; ischemic postconditioning; myocardial protection; rabbit
- 分类号:
- R542.2
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的: 探讨缺血后适应减轻家兔急性缺血/再灌注损伤的作用。方法: 将56只大耳白兔随机分为对照组(n=28)及缺血后适应组(n=28)。采用夹闭左室支40 min,再灌注3 h方法建立兔急性心肌梗死-再灌注模型。对照组不施加干预，缺血后适应组于再灌注开始初再次缺血30 s、再灌注30 s，连续重复3次循环后，恢复冠脉血流，观察两组兔于再灌注前至再灌注后2 h期间心电的变化；并测定缺血前、灌注0 h、1 h及3 h血清丙二醛（MDA）、超氧化物岐化酶（SOD）及谷胱甘肽过氧化物酶（GSH-PX）水平的变化。实验结束后，两组中各随机处死半数兔用伊文氏蓝及氯化三苯基四氮唑红（TTC）染色法，测定心肌梗死的面积；另半数兔于4 周后进行经胸心脏超声心动图检查。结果: 缺血后适应组再灌注2 h末心肌再灌注的有效率（心肌获得有效再灌注的百分比率）高于对照组(P<0.05)；而心肌梗死的面积低于对照组(P<0.05)。缺血后适应组再灌注1 h血清MDA的水平低于对照组；SOD、GSH-PX的活性高于对照组(P<0.05)。心肌梗死4周后，心脏超声检查缺血后适应组左室后壁室壁的厚度及收缩期室壁增厚率△T均明显高于对照组(P<0.05)；左室射血分数(LVEF)、左室缩短分数(LVFS)较对照组明显改善(P<0.05)。结论: 缺血后适应可通过抑制再灌注早期氧自由基的活化，减轻心肌急性缺血/再灌注损伤，改善心肌的有效灌注，降低心肌梗死的面积及减轻心梗近期（恢复期）心脏结构与功能的损害。
- Abstract:
- AIM: To study the early protective effect of myocardium by ischemic postconditioning on ischemic myocardium in rabbits. METHODS: Fifty six rabbits were included in this study and were randomly divided into control group (Con, n=28) and ischemic postconditioning group (Post-con, n=28). An in vivo rabbit model of acute myocardial infarction/reperfusion was established with left ventricle branch (LVB) occluded for 40 min and reperfused for 3 h. In Con, there was no intervention. In Post-con, at the start of R, three cycles of 30 sec R and 30 sec LVB re-occlusion preceded the 3 h of R. ECG was observed during the first 2 h of reperfusion. Plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were measured at baseline, end of ischemia, and at 1h and 3 h of reperfusion. At the end of the experiment, the rabbits of Con and Post-con were randomly divided into two equal subgroups. The rabbits in one subgroup were killed to determine myocardial infarct size determined by dual staining with triphenyltetrazolium chloride and Evans blue dye. Cardiac structural and functional changes were evaluated with transthoracic echocardiography (TTE) in the other subgroup 4 weeks after myocardial infarction. RESULTS: Myocardial reperfusion was much more effective in Post-con group vs. Con (P<0.05) and myocardial infarct size was significantly reduced in Post-con vs. Con (P<0.05). Plasma MDA at 1 h of reperfusion was significantly less and plasma SOD and GSH-PX were higher in Post-con vs. Con (P<0.05). After 4 weeks, TTE showed that the extent of posterior left ventricular (PLV) wall and its thickenness in systolic period as well as left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were significantly improved in Post-con vs. Con (P<0.05). CONCLUSION: Ischemic postconditioning reduces acute myocardial ischemia/reperfusion injury by inhibiting oxyradical activation at the beginning of reperfusion, which improves the effective perfusion on ischemic myocardium and reduces myocardial infarct size and improves left ventricular contractive function.
参考文献/References
［1］ Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning［J］. Am J Physiol Heart Circ Physiol, 2003, 285(2):H579-H588.
［2］ Staat P, Rioufol G, Piot C, et al. Postconditioning the Human Heart［J］. Circulation, 2005, 112(14):2143-2148.
［3］ 李国营，田素民，于连发，等. 兔心肌缺血及缺血再灌注模型的制备［J］. 解剖学研究, 2002, 24(3):237－239.
［4］ Murry CE, Jennings RB, Reimer KA. Preconditiong with ischemia: a delay of lethal cell injury in ischemic myocardium［J］. Circulation, 1986, 74(5):1124-1136.
［5］ Dow J, Bhandari A, Kloner RA. Ischemic postconditioning's benefit on reperfusion ventricular arrhythmias is maintained in the senescent heart［J］. J Cardiovasc Pharmacol Ther, 2008, 13(2):141-148.
［6］ Santoro GM, Valenti R, Buonamici P, et al. Relation between ST-segment changes and myocardial perfusion evaluated by myocardial contrast echocardiography in patient with acute myocardial infarction treatod with direct angioplasty［J］. Am J Cardiol, 1998, 82(8):932-937.
［7］ 郭莲怡，刘仁光. 兔心肌缺血再灌注心电图分析［J］. 心电学杂志, 2003, 22(2):84-87.
［8］ Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia reperfusion injury by inhibiting events in the early minutes of reperfusion［J］. Cardiovasc Res, 2004, 62(1):74-85.
［9］ Zhao ZQ, Zang YM. Alternative cardioprotective strategy during reperfusion: postconditioning vs preconditioning［J］. 心脏杂志, 2006, 18(1):1-7,13.
［10］Sato H, Zhao ZQ, McGee DS, et al. Supplemental L-arginine during cardioplegic arrest and reperfusion avoids regional postischemic injury［J］. J Thorac Cardiovasc Surg, 1995, 110(2):302-314.
［11］Toyoda Y, Di Gregorio V, Parker RA, et al. Anti-stunning and anti-infarct effects of adenosine -enhanced ischemic precondintioning［J］. Circulation, 2000, 102(19 Suppl 3): III326-III331.
［12］Thibault H, Piot C, Staat P, et al. Long-term benefit of postconditioning［J］. Circulation, 2008, 117(8):1037-1044.
备注/Memo
- 备注/Memo:
- 收稿日期：2008-11-13.基金项目：福建省自然科学基金项目资助（2007J0298） 通讯作者：林荣，主任医师，教授，主要从事冠脉介入和电生理研究Email:qzlinrong@163.com 作者简介：王凌，主治医师，硕士Email：wang-qz@tom.com
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