What is the clinical evidence from this study?

Study design: 其他. Population: 心律失常与氧化应激. Intervention: H2O2（氧化应激） vs. 溶媒. Primary outcome: 2 分钟时 WT 心肌细胞 90% 复极化时的动作电位时程（APD90） (p=0.0006).

What does this research mean for the field?

Exposure to oxidative stress prolongs action potential duration and increases early afterdepolarizations in murine cardiomyocytes through the inhibition of potassium currents by oxidation-activated protein kinase A type I. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

October 9, 2020AJP Heart and Circulatory Physiology18 citationsOpen Access

氧化激活的蛋白激酶A抑制心脏钾电流可导致心脏早期后除极

MTMaximilian TrumUniversity Hospital Regensburg MIMd. Monirul IslamUniversity of Dhaka SLSimon LebekElectrophysiology

Key Result

暴露于 H2O2 可显著延长野生型小鼠心肌细胞的动作电位时程并增加早期后除极，而该效应在氧化还原缺陷型 PKA 敲入小鼠中消失。

Study Design

Type

其他

Structured PICO

Population

小鼠心室肌细胞

Intervention

氧化激活的 I 型 PKA

Outcome

瞬时外向钾电流（I to）和内向整流钾电流（I K1）的抑制、APD 延长以及早期后除极的发生surrogate

氧化激活的 I 型 PKA 在 ROS 诱导的小鼠心肌细胞动作电位延长和早期后除极中发挥机制性作用。

Main Result

Absolute Event Rate: 107.6% vs 53.42%

p-value: p=0.0006

Limitations

H2O2 exposure does not result in a selective oxidation of PKA, as there are many other targets for ROS-dependent oxidation.
The use of BaCl2 to inhibit IK1 is voltage-dependent, which could lead to an underestimation of IK1 at more positive membrane potentials.
Species differences in the contribution of Ito to membrane repolarization between murine and human ventricular myocytes.

Abstract

氧化激活的 I 型 PKA 可抑制瞬时外向钾电流（I to）和内向整流钾电流（I K1），并促进 ROS 诱导的小鼠心室肌细胞 APD 延长以及早期后除极的发生。

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