...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Elevated potassium outward currents in hyperoxia treated atrial cardiomyocytes
【24h】

Elevated potassium outward currents in hyperoxia treated atrial cardiomyocytes

机译：在氧过多向外高钾电流治疗心房心肌细胞

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

Supplementation of 100% oxygen is a very common intervention in intensive care units (ICU) and critical care centers for patients with dysfunctional lung and lung disorders. Although there is advantage in delivering sufficient levels of oxygen, hyperoxia is reported to be directly associated with increasing in‐hospital deaths. Our previous studies reported ventricular and electrical remodeling in hyperoxia treated mouse hearts, and in this article, for the first time, we are investigating the effects of hyperoxia on atrial electrophysiology using whole‐cell patch‐clamp electrophysiology experiments along with assessment of Kv1.5, Kv4.2, and KChIP2 transcripts and protein profiles using real‐time quantitative RT‐PCR and Western blotting. Our data showed that induction of hyperoxia for 3 days in mice showed larger outward potassium currents with shorter action potential durations (APD). This increase in current densities is due to significant increase in ultrarapid delayed rectifier outward K + currents ( I Kur ) and rapidly activating, rapidly inactivating transient outward K+ current ( I to ) densities. We also observed a significant increase in both transcripts and protein levels of Kv1.5 and KChIP2 in hyperoxia treated atrial cardiomyocytes, whereas no significant change was observed in Kv4.2 transcripts or protein. The data presented here further support our previous findings that hyperoxia induces not only ventricular remodeling, but also atrial electrical remodeling.
机译：100%的氧气是一种很常见的补充在重症监护病房(ICU)和干预患者的急救护理中心功能失调的肺癌和肺部疾病。在提供足够的有优势据报道,水平的氧,氧过多与增加住院量直接相关人死亡。和电气改造在氧过多治疗老鼠心脏,在本文中,第一时间,我们正在调查的影响使用氧过多对心房电生理整个检测细胞片夹电生理学Kv1.5实验与评估,Kv4.2, KChIP2转录和蛋白质配置文件使用实时定量RT PCR和西方墨点法。3天的氧过多大老鼠外向钾电流较短的行动潜在的持续时间(adp)。电流密度将显著增加在超速的延迟整流K +电流(科尔)和快速激活,快速灭活瞬态向外K +电流(我)密度。成绩单和显著增加蛋白质含量的Kv1.5和KChIP2氧过多治疗心房心肌细胞,而没有在Kv4.2观察显著变化成绩单或蛋白质。进一步支持我们先前的发现不仅氧过多诱发心室重构,而且心房电重构。

著录项

相似文献

  • 外文文献
  • 中文文献
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