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“氯离子理论”,一种关于心力衰竭病理生理学中肾脏处理和体液分布的统一假说。

The "chloride theory", a unifying hypothesis for renal handling and body fluid distribution in heart failure pathophysiology.

作者信息

Kataoka Hajime

机构信息

Internal Medicine, Nishida Hospital, Oita, Japan.

出版信息

Med Hypotheses. 2017 Jul;104:170-173. doi: 10.1016/j.mehy.2017.06.005. Epub 2017 Jun 8.

DOI:10.1016/j.mehy.2017.06.005
PMID:28673579
Abstract

Body fluid volume regulation is a complex process involving the interaction of various afferent (sensory) and neurohumoral efferent (effector) mechanisms. Historically, most studies focused on the body fluid dynamics in heart failure (HF) status through control of the balance of sodium, potassium, and water in the body, and maintaining arterial circulatory integrity is central to a unifying hypothesis of body fluid regulation in HF pathophysiology. The pathophysiologic background of the biochemical determinants of vascular volume in HF status, however, has not been known. I recently demonstrated that changes in vascular and red blood cell volumes are independently associated with the serum chloride concentration, but not the serum sodium concentration, during worsening HF and its recovery. Based on these observations and the established central role of chloride in the renin-angiotensin-aldosterone system, I propose a unifying hypothesis of the "chloride theory" for HF pathophysiology, which states that changes in the serum chloride concentration are the primary determinant of changes in plasma volume and the renin-angiotensin-aldosterone system under worsening HF and therapeutic resolution of worsening HF.

摘要

体液容量调节是一个复杂的过程,涉及各种传入(感觉)和神经体液传出(效应)机制的相互作用。从历史上看,大多数研究通过控制体内钠、钾和水的平衡来关注心力衰竭(HF)状态下的体液动力学,而维持动脉循环完整性是HF病理生理学中体液调节统一假说的核心。然而,HF状态下血管容量生化决定因素的病理生理背景尚不清楚。我最近证明,在HF恶化及其恢复过程中,血管和红细胞容量的变化与血清氯浓度独立相关,而与血清钠浓度无关。基于这些观察结果以及氯在肾素-血管紧张素-醛固酮系统中已确立的核心作用,我提出了一个关于HF病理生理学的“氯理论”统一假说,该假说指出,血清氯浓度的变化是HF恶化及HF恶化治疗缓解时血浆容量和肾素-血管紧张素-醛固酮系统变化的主要决定因素。

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