...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Circulation journal >Ischemia-Induced Norepinephrine Release, but not Norepinephrine-Derived Free Radicals, Contributes to Myocardial Ischemia - Reperfusion Injury.
【24h】

Ischemia-Induced Norepinephrine Release, but not Norepinephrine-Derived Free Radicals, Contributes to Myocardial Ischemia - Reperfusion Injury.

机译：缺血诱导的去甲肾上腺素释放，而不是去甲肾上腺素衍生的自由基不参与心肌缺血-再灌注损伤。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemia -reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the present study. Methods and Results Cardiac sympathetic denervation was produced in Wistar rats by a solution of 10% phenol 1 week before ischemia. Atenolol (0.5 mg/kg) was intravenously administered 10 min before the coronary occlusion. The left coronary artery was occluded for 30 min and thereafter reperfused. Cardiac interstitial fluid was collected by a microdialysis probe and free radicals in dialysate were determined by electron paramagnetic resonance (EPR) spin trapping, using 5,5-dimethyl-1-pyrroline-N-oxide as a spin trap. The ratio of infarct size to the ischemic area at risk (I/R) was decreased in both the phenol and atenolol groups compared with control (28.5+/-11.3, 31.8+/-10.7 vs 50.6+/-14.7%, p<0.05). During the coronary occlusion, concentrations of interstitial NE increased markedly in the control and atenolol groups, but was unchanged in the phenol group. EPR signal intensity (relative value to internal standard) was maximal at 1 h after reperfusion and was similar in the phenol and control groups (0.32+/-0.15 vs 0.45+/-0.19). Conclusions Cardiac denervation protected myocyte against ischemia - reperfusion injury through decreasing direct NE toxicity, but not through decreasing NE-derived free radicals. (Circ J 2005; 69: 590 - 595).
机译：背景：去甲肾上腺素（NE）衍生的自由基可能导致缺血再灌注后的心肌细胞损伤，因此，本研究研究了交感神经支配对心肌缺血再灌注损伤的影响。方法和结果缺血前1周，Wistar大鼠通过10％苯酚溶液产生心脏交感神经去神经。在冠状动脉闭塞前10分钟静脉注射阿替洛尔（0.5 mg / kg）。闭塞左冠状动脉30分钟，然后再灌注。用5,5-二甲基-1-吡咯啉-N-氧化物作为自旋阱，通过微透析探针收集心脏组织液，并通过电子顺磁共振（EPR）自旋阱测定透析液中的自由基。与对照组相比，苯酚和阿替洛尔组梗塞面积与危险缺血区域的比率（I / R）均降低（28.5 +/- 11.3、31.8 +/- 10.7和50.6 +/- 14.7％，p < 0.05）。在冠状动脉闭塞过程中，对照组和阿替洛尔组间质NE的浓度显着增加，而苯酚组则没有变化。 EPR信号强度（相对于内标物的相对值）在再灌注后1 h达到最大值，在苯酚组和对照组中相似（0.32 +/- 0.15 vs 0.45 +/- 0.19）。结论心脏去神经可通过减少直接NE毒性而不是通过减少NE衍生的自由基来保护心肌细胞免受缺血-再灌注损伤。 （Circ J 2005; 69：590-595）。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号