Elevated potassium outward currents in hyperoxia treated atrial cardiomyocytes.
Elevated potassium outward currents in hyperoxia treated atrial cardiomyocytes.
复制标题
高氧处理的心房心肌细胞中钾外向电流升高。
DOI：
10.1002/jcp.26263
复制
发表时间：
2018
影响因子：
5.6
通讯作者：
Panguluri,SivaK
中科院分区：
文献类型：
--
作者：
Vysotskaya,Zhanna;Chidipi,Bojjibabu;Rodgers,JenniferL;Tang,Xiaolan;Samal,Eva;Kolliputi,Narasaiah;Mohapatra,Subhra;Bennett,EricS;Panguluri,SivaK
在重症监护病房（ICU）和重症监护中心，对肺功能失调和肺部疾病患者，补充100%氧气是一种非常常见的干预措施。尽管提供足量的氧气有优势，但据报道，高氧与院内死亡增加直接相关。我们之前的研究报道了高氧处理小鼠心脏的心室和电重构，在这篇文章中，我们首次使用全细胞膜片钳电生理实验研究了高氧对心房电生理的影响，并使用实时定量RT - PCR和Western blotting评估了Kv1.5、Kv4.2和KChIP2转录物和蛋白质谱。我们的数据显示，诱导小鼠高氧3天后，向外钾电流增大，动作电位持续时间（APD）缩短。电流密度的增加是由于超快速延迟整流器向外K+电流（IKur）和快速激活、快速灭活瞬态外向K+电流（Ito）密度的显著增加。我们还观察到，在高氧处理的心房心肌细胞中，Kv1.5和KChIP2的转录本和蛋白质水平均显著增加，而Kv4.2的转录本或蛋白质水平没有显著变化。本研究的数据进一步支持了我们之前的发现，即高氧不仅诱导心室重构，还诱导心房电重构。
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 (IKur) and rapidly activating, rapidly inactivating transient outward K+ current (Ito) 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.