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间质钠离子在心力衰竭中的病理生理作用。

The pathophysiological role of interstitial sodium in heart failure.

机构信息

Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.

Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium.

出版信息

J Am Coll Cardiol. 2015 Feb 3;65(4):378-388. doi: 10.1016/j.jacc.2014.11.025.

DOI:10.1016/j.jacc.2014.11.025
PMID:25634838
Abstract

The current understanding of heart failure (HF) does not fully explain the spectrum of HF symptoms. Most HF hospitalizations are related to sodium (Na(+)) and fluid retention resulting from neurohumoral up-regulation. Recent insights suggest that Na(+) is not distributed in the body solely as a free cation, but that it is also bound to large interstitial glycosaminoglycan (GAG) networks in different tissues, which have an important regulatory function. In HF, high Na(+) intake and neurohumoral alterations disrupt GAG structure, leading to loss of the interstitial buffer capacity and disproportionate interstitial fluid accumulation. Moreover, a diminished endothelial GAG network (the endothelial glycocalyx) results in increased vascular resistance and disturbed endothelial nitric oxide production. New imaging modalities can help evaluate interstitial Na(+) and endothelial glycocalyx integrity. Furthermore, several therapies have been proven to stabilize interstitial GAG networks. Hence, a better appreciation of this new Na(+) "compartment" might improve current management of HF.

摘要

目前对心力衰竭(HF)的认识还不能完全解释 HF 症状的全貌。大多数 HF 住院是与神经体液上调导致的钠(Na(+))和液体潴留有关。最近的研究结果表明,Na(+)在体内不仅仅以游离阳离子的形式分布,而且还与不同组织中的大型间质糖胺聚糖(GAG)网络结合,这些网络具有重要的调节功能。在 HF 中,高 Na(+)摄入和神经体液改变会破坏 GAG 结构,导致间质缓冲能力丧失和不成比例的间质液积聚。此外,内皮 GAG 网络(内皮糖萼)减少会导致血管阻力增加和内皮一氧化氮产生紊乱。新的成像方式可以帮助评估间质 Na(+)和内皮糖萼的完整性。此外,已经有几种疗法被证明可以稳定间质 GAG 网络。因此,更好地了解这个新的 Na(+)“隔室”可能会改善 HF 的当前治疗方法。

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