Kawaguchi Satoshi, Okada Motoi
Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Bloomington, IN 46202, USA.
Department of Emergency Medicine, Asahikawa Medical University, Asahikawa 078-8510, Japan.
Metabolites. 2021 Dec 6;11(12):846. doi: 10.3390/metabo11120846.
The mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. These factors inhibit the production of ATP, essential for myocardial energy metabolism, resulting in cardiac dysfunction. This review focuses on the metabolic changes in sepsis, particularly in the heart. In addition to managing inflammation, interventions focusing on metabolism may be a new therapeutic strategy for cardiac dysfunction due to sepsis.
脓毒症诱发的心脏功能障碍机制被认为与心肌缺血不同。在脓毒症中,化学介质,如内毒素、细胞因子和一氧化氮,会导致代谢异常、线粒体功能障碍以及β-肾上腺素能受体下调。这些因素抑制了对心肌能量代谢至关重要的ATP生成,从而导致心脏功能障碍。本综述聚焦于脓毒症中的代谢变化,尤其是心脏中的代谢变化。除了控制炎症外,针对代谢的干预措施可能是治疗脓毒症所致心脏功能障碍的一种新的治疗策略。