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脓毒症性心肌病中心脏代谢——心脏异常代谢功能障碍

Heart Metabolism in Sepsis-Induced Cardiomyopathy-Unusual Metabolic Dysfunction of the Heart.

机构信息

Chair of Internal Medicine and Department of Internal Medicine in Nursing, Faculty of Health Sciences, Medical University of Lublin, 20-093 Lublin, Poland.

Doctoral School, Medical University of Lublin, 20-093 Lublin, Poland.

出版信息

Int J Environ Res Public Health. 2021 Jul 16;18(14):7598. doi: 10.3390/ijerph18147598.

DOI:10.3390/ijerph18147598
PMID:34300048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8303349/
Abstract

Due to the need for continuous work, the heart uses up to 8% of the total energy expenditure. Due to the relatively low adenosine triphosphate (ATP) storage capacity, the heart's work is dependent on its production. This is possible due to the metabolic flexibility of the heart, which allows it to use numerous substrates as a source of energy. Under normal conditions, a healthy heart obtains approximately 95% of its ATP by oxidative phosphorylation in the mitochondria. The primary source of energy is fatty acid oxidation, the rest of the energy comes from the oxidation of pyruvate. A failed heart is characterised by a disturbance in these proportions, with the contribution of individual components as a source of energy depending on the aetiology and stage of heart failure. A unique form of cardiac dysfunction is sepsis-induced cardiomyopathy, characterised by a significant reduction in energy production and impairment of cardiac oxidation of both fatty acids and glucose. Metabolic disorders appear to contribute to the pathogenesis of cardiac dysfunction and therefore are a promising target for future therapies. However, as many aspects of the metabolism of the failing heart remain unexplained, this issue requires further research.

摘要

由于需要持续工作,心脏消耗的能量占总能量消耗的 8%。由于三磷酸腺苷(ATP)的储存量相对较低,心脏的工作依赖于其产生。这是由于心脏的代谢灵活性,它允许它使用许多底物作为能量来源。在正常情况下,健康的心脏通过线粒体中的氧化磷酸化获得大约 95%的 ATP。能量的主要来源是脂肪酸氧化,其余的能量来自丙酮酸的氧化。衰竭的心脏的特点是这些比例的紊乱,作为能量来源的各个成分的贡献取决于病因和心力衰竭的阶段。一种独特的心脏功能障碍形式是脓毒症性心肌病,其特征是能量产生显著减少,以及脂肪酸和葡萄糖的心脏氧化受损。代谢紊乱似乎导致了心脏功能障碍的发病机制,因此是未来治疗的一个有前途的靶点。然而,由于衰竭心脏的许多代谢方面仍未得到解释,这个问题需要进一步的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/52ecfb58b810/ijerph-18-07598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/bd97aa64dcaa/ijerph-18-07598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/1be4edd0f640/ijerph-18-07598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/52ecfb58b810/ijerph-18-07598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/bd97aa64dcaa/ijerph-18-07598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/1be4edd0f640/ijerph-18-07598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e708/8303349/52ecfb58b810/ijerph-18-07598-g003.jpg

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