Long-term inhibition of myocardial infarction by postconditioning during reperfusion
Long-term inhibition of myocardial infarction by postconditioning during reperfusion
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DOI：
10.1007/s00395-006-0625-0
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发表时间：
2007-01-01
影响因子：
9.5
通讯作者：
Zhao, Zhi-Qing
中科院分区：
文献类型：
--
作者：
Mykytenko, James;Kerendi, Faraz;Zhao, Zhi-Qing
在短时间再灌注后，后处理的脑保护作用已得到充分证明。本研究验证了长期再灌注后，后处理可减少梗死面积、血管功能障碍和中性粒细胞聚集的假设。实验动物分为两组，对照组（再灌注3 h或24 h）和后处理组（再灌注3 h或24 h）。缺血期间危险区（AAR）和侧支血流的大小在各组之间相似。在对照组中，梗死面积占AAR的百分比（30 +/- 3 vs. 39 +/- 2* %）通过TTC染色，通过光泽精增强化学发光从缺血后冠状动脉产生超氧阴离子[（89 +/- 5 vs. 236 +/- 27* 相对光单位（RLU/mg）]，再灌注3至24小时期间，AAR中免疫组织化学染色显示中性粒细胞（PMN）积聚（52 +/- 11 vs. 84 +/- 14* 细胞/mm（2）心肌）显着增加。与时间匹配的对照组相比，后处理减少了3和24 h再灌注组的梗死面积（15 +/-4 dagger和27 +/- 3.6 dagger %）、超氧阴离子生成（24 +/- 4 dagger和43 +/- 11 dagger RLU/mg）和PMN积聚（19 +/- 6 dagger和45 +/- 8 dagger细胞/mm（2）心肌）。这些数据表明，心肌损伤的再灌注持续时间增加，减少梗死面积和衰减炎症反应与后处理后持续时间长的再灌注。* p < 0.05，24小时相对于3小时对照;匕首p < 0.05，后处理相对于时间匹配的对照。
Cardioprotection with postconditioning has been well demonstrated after a short period of reperfusion. This study tested the hypothesis that postconditioning reduces infarct size, vascular dysfunction, and neutrophil accumulation after a long-term reperfusion. Canines undergoing 60 min left anterior descending artery (LAD) occlusion were divided into two control groups of either 3 h or 24 h of full reperfusion and two postconditioning groups with three 30 s cycles of reperfusion and re-occlusion applied at the onset of either 3 h or 24 h of reperfusion. Size of the area at risk (AAR) and collateral blood flow during ischemia were similar among groups. In controls, infarct size as percentage of the AAR (30 +/- 3 vs. 39 +/- 2* %) by TTC staining, superoxide anion generation from the post-ischemic coronary arteries by lucigenin-enhanced chemiluminescence [(89 +/- 5 vs. 236 +/- 27* relative light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical staining in the AAR (52 +/- 11 vs. 84 +/- 14* cells/mm(2) myocardium) significantly increased between 3 and 24 h of reperfusion. Postconditioning reduced infarct size (15 +/- 4 dagger and 27 +/- 3.6 dagger %), superoxide anion generation (24 +/- 4 dagger and 43 +/- 11 dagger RLU/mg), and PMN accumulation (19 +/- 6 dagger and 45 +/- 8 dagger cells/mm(2) myocardium) in the 3 and 24 h reperfusion groups relative to time-matched controls. These data suggest that myocardial injury increases with duration of reperfusion; reduction in infarct size and attenuation in inflammatory responses with postconditioning persist after a prolonged reperfusion. * p < 0.05 24 vs. 3 h control; dagger p < 0.05 postconditioning vs. time-matched control.