首页> 外文会议>International Society for Heart Research.Congress >Reactive Oxygen Species, Na+/h+ Exchange and Ca2+ Overload During Myocardial Ischemia/reperfusion injury: the Paradox Explained?
【24h】

Reactive Oxygen Species, Na+/h+ Exchange and Ca2+ Overload During Myocardial Ischemia/reperfusion injury: the Paradox Explained?

机译:心肌缺血/再灌注损伤期间,活性氧物质,Na + / h +交换和Ca2 +过载:悖论解释了吗?

获取原文

摘要

Summary. Reperfusion of the myocardium following an ischemic episode is associated with profound contractile and metabolic dysfunction. Reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and hydroxyl ("OH) radicals, are produced during reperfusion after a transient ischemic attack of the myocardium. Reperfusion is also associated with the activation of the cardiac Na+/H+ exchanger isoform-1 (NHE-1), which restores intracellular pH (pHi) towards normal following ischemia-induced acidosis. Activation of NHE-1 also produces undesirable secondary effects leading to the exacerbation of tissue injury, a phenomenon termed the "pH paradox". Increased generation of ROS plays an important role in reperfusion-induced myocardial stunning and NHE-1 activation. However, the exact relationship between ROS, NHE-1 activity and intracellular Ca2+ overload has not been defined. Recent development of new, more specific. NHE-1 inhibitors has enhanced our understanding of the link between ROS burst, the pH paradox, and Ca2+ overload during I/R injury.
机译:概括。在缺血性插曲后对心肌的再灌注与深刻的收缩和代谢功能障碍有关。在心肌的短暂缺血性发作后,在再灌注过程中产生反应性氧物质(ROS),例如过氧化氢(H 2 O 2)和羟基(“OH)基团。再灌注也与心脏Na + / H +交换剂同种型的激活相关-1(NHE-1),其将细胞内pH(PHI)恢复到正常培养的酸中毒后。NHE-1的活化也产生了不希望的二次效应,导致组织损伤的加剧,称为“pHARADOX”的现象。 ROS的生成增加起着再灌注引起的心肌顿抑和NHE-1活化中起重要作用。但是,ROS,NHE-1活性之间和细胞内Ca2 +超载尚未定义的确切关系。新的,更具体的研究进展。NHE -1抑制剂提高了我们对ROS突发,pH悖论和CA2 +在I / R损伤期间的联系之间的理解。

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