Abstract
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.
Highlights
This review focuses on the current knowledge of metabolic alteration in sepsis, especially the dysregulation of cardiac metabolism
Our findings demonstrated that (1) β3AR is increased in septic hearts; (2) β3AR blockade preserves cardiac adenosine triphosphate (ATP) through the improvement of FAO; (3) β3AR blockade prevents lipid accumulation in the myocardium; and (4) β3AR regulates inducible NO synthase (iNOS)
This review focuses on cardiac metabolism in sepsis
Summary
Cardiovascular abnormalities in sepsis have been known since the 1950s [8], Parker et al reported that intrinsic myocardial dysfunction, with an increased volume and a decreased ejection fraction, in patients with sepsis is reversible [9] These functional changes in the left ventricle were observed 7–10 days from the onset in survivors, whereas they were less profound in non-survivors [9,10]. Some clinical researchers suggested that cardiac dysfunction in sepsis is strongly associated with mortality [16,17,18,19] These different conclusions might result from the complexity of the disease, patient characteristics, methods of diagnosis, and disease access.
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