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质子量子隧穿:对酸中毒诱导的心律失常/心脏骤停的影响及相关性

Proton Quantum Tunneling: Influence and Relevance to Acidosis-Induced Cardiac Arrhythmias/Cardiac Arrest.

作者信息

Ababneh Omar, Qaswal Abdallah Barjas, Alelaumi Ahmad, Khreesha Lubna, Almomani Mujahed, Khrais Majdi, Khrais Oweiss, Suleihat Ahmad, Mutleq Shahed, Al-Olaimat Yazan, Nawafleh Sager

机构信息

Department of Anesthesia and Intensive Care, School of Medicine, The University of Jordan, Amman 11942, Jordan.

Department of Internal Medicine, School of Medicine, The University of Jordan, Amman 11942, Jordan.

出版信息

Pathophysiology. 2021 Sep 3;28(3):400-436. doi: 10.3390/pathophysiology28030027.

Abstract

Acidosis and its associated pathologies predispose patients to develop cardiac arrhythmias and even cardiac arrest. These arrhythmias are assumed to be the result of membrane depolarization, however, the exact mechanism of depolarization during acidosis is not well defined. In our study, the model of quantum tunneling of protons is used to explain the membrane depolarization that occurs during acidosis. It is found that protons can tunnel through closed activation and inactivation gates of voltage-gated sodium channels Nav1.5 that are present in the membrane of cardiac cells. The quantum tunneling of protons results in quantum conductance, which is evaluated to assess its effect on membrane potential. The quantum conductance of extracellular protons is higher than that of intracellular protons. This predicts an inward quantum current of protons through the closed sodium channels. Additionally, the values of quantum conductance are influential and can depolarize the membrane potential according to the quantum version of the GHK equation. The quantum mechanism of depolarization is distinct from other mechanisms because the quantum model suggests that protons can directly depolarize the membrane potential, and not only through indirect effects as proposed by other mechanisms in the literature. Understanding the pathophysiology of arrhythmias mediated by depolarization during acidosis is crucial to treat and control them and to improve the overall clinical outcomes of patients.

摘要

酸中毒及其相关病理状况使患者易发生心律失常甚至心脏骤停。这些心律失常被认为是膜去极化的结果,然而,酸中毒期间去极化的确切机制尚不清楚。在我们的研究中,质子量子隧穿模型被用于解释酸中毒期间发生的膜去极化。研究发现,质子可以隧穿穿过心肌细胞膜上存在的电压门控钠通道Nav1.5的关闭的激活门和失活门。质子的量子隧穿导致量子电导,通过评估量子电导来评估其对膜电位的影响。细胞外质子的量子电导高于细胞内质子的量子电导。这预示着质子通过关闭的钠通道有内向量子电流。此外,量子电导的值具有影响力,并且可以根据GHK方程的量子版本使膜电位去极化。去极化的量子机制与其他机制不同,因为量子模型表明质子可以直接使膜电位去极化,而不仅仅是通过文献中其他机制所提出的间接效应。了解酸中毒期间由去极化介导的心律失常的病理生理学对于治疗和控制它们以及改善患者的整体临床结局至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb83/8830476/57e199bb9b53/pathophysiology-28-00027-g001.jpg

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