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Basic science and research
Sepsis-induced cardiac dysfunction: a review of pathophysiology
Reverien Habimana, Insu Choi, Hwa Jin Cho, Dowan Kim, Kyoseon Lee, Inseok Jeong
Acute Crit Care. 2020;35(2):57-66.   Published online May 31, 2020
DOI: https://doi.org/10.4266/acc.2020.00248
  • 13,490 View
  • 906 Download
  • 43 Web of Science
  • 48 Crossref
AbstractAbstract PDF
It is well known that cardiac dysfunction in sepsis is associated with significantly increased mortality. The pathophysiology of sepsis-induced cardiac dysfunction can be summarized as involving impaired myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Impaired blood flow to the myocardium is associated with microvascular dysfunction, impaired endothelium, and ventriculo-arterial uncoupling. The mechanisms behind direct myocardial depression consist of downregulation of β-adrenoceptors and several myocardial suppressants (such as cytokine and nitric oxide). Recent research has highlighted that mitochondrial dysfunction, which results in energy depletion, is a major factor in sepsis-induced cardiac dysfunction. Therefore, the authors summarize the pathophysiological process of cardiac dysfunction in sepsis based on the results of recent studies.

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Review
Basic science and research
Role of Mitochondrial Oxidative Stress in Sepsis
Harsha Nagar, Shuyu Piao, Cuk-Seong Kim
Acute Crit Care. 2018;33(2):65-72.   Published online May 31, 2018
DOI: https://doi.org/10.4266/acc.2018.00157
  • 10,499 View
  • 436 Download
  • 55 Web of Science
  • 59 Crossref
AbstractAbstract PDF
Mitochondria are considered the power house of the cell and are an essential part of the cellular infrastructure, serving as the primary site for adenosine triphosphate production via oxidative phosphorylation. These organelles also release reactive oxygen species (ROS), which are normal byproducts of metabolism at physiological levels; however, overproduction of ROS under pathophysiological conditions is considered part of a disease process, as in sepsis. The inflammatory response inherent in sepsis initiates changes in normal mitochondrial functions that may result in organ damage. There is a complex system of interacting antioxidant defenses that normally function to combat oxidative stress and prevent damage to the mitochondria. It is widely accepted that oxidative stress-mediated injury plays an important role in the development of organ failure; however, conclusive evidence of any beneficial effect of systemic antioxidant supplementation in patients with sepsis and organ dysfunction is lacking. Nevertheless, it has been suggested that antioxidant therapy delivered specifically to the mitochondria may be useful.

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ACC : Acute and Critical Care