Sepsis-Induced Cardiomyopathy: Oxidative Implications in the Initiation and Resolution of the Damage.

Vasiliki Tsolaki,Demosthenes Makris,Epameinontas Zakynthinos,Konstantinos Mantzarlis

doi:10.1155/2017/7393525

Vasiliki Tsolaki, Demosthenes Makris + Show 2 more

Open Access

https://doi.org/10.1155/2017/7393525

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Abstract

Cardiac dysfunction may complicate the course of severe sepsis and septic shock with significant implications for patient's survival. The basic pathophysiologic mechanisms leading to septic cardiomyopathy have not been fully clarified until now. Disease-specific treatment is lacking, and care is still based on supportive modalities. Septic state causes destruction of redox balance in many cell types, cardiomyocytes included. The production of reactive oxygen and nitrogen species is increased, and natural antioxidant systems fail to counterbalance the overwhelming generation of free radicals. Reactive species interfere with many basic cell functions, mainly through destruction of protein, lipid, and nucleic acid integrity, compromising enzyme function, mitochondrial structure and performance, and intracellular signaling, all leading to cardiac contractile failure. Takotsubo cardiomyopathy may result from oxidative imbalance. This review will address the multiple aspects of cardiomyocyte bioenergetic failure in sepsis and discuss potential therapeutic interventions.

Highlights

Myocardial depression may develop in patients with severe sepsis and septic shock, complicating the course of their disease
It has been found that both superoxide dismutase and glutathione peroxidase activities, in cardiac mitochondria, decrease early after sepsis induction and remain at lower levels throughout the first 24 hours after LPS challenge. These findings suggest that sepsis depletes mitochondria of their defense mechanisms against reactive oxygen species (ROS) [53]
An antioxidant, anti-inflammatory, and antiapoptotic flavanone glycoside found in grapefruits and oranges, when given orally in septic mouse models, regulated the expression and release of superoxide dismutase (SOD) and malondialdehyde (MDA) to inhibit the subsequent myocardial oxidative stress, suppressed myocardial cell apoptosis, and ameliorated heart morphological changes, all these leading to improved mouse survival [115]

Summary

Introduction

Myocardial depression may develop in patients with severe sepsis and septic shock, complicating the course of their disease. Hypoxia and acidosis, hypotension and hypovolemia, metabolic disturbances, coagulation abnormalities, and increased production of reactive oxygen and nitrogen species (ROS and RNS) have been proposed to participate in myocardial depression during sepsis [5]. The majority of body oxygen is taken up by the mitochondria and is used for energy production (in the form of adenosine triphosphate (ATP)) It appears that these organelles may play a pivotal role in the pathogenesis of sepsis-induced organ dysfunction. Reactive oxygen and nitrogen species are produced in excess and have been implicated in the genesis of sepsis-induced myocardial dysfunction [10,11,12,13,14,15,16]. We will focus on the role of reactive oxygen and nitrogen species in the generation of myocardial dysfunction in sepsis. We focused on the rest 127 clinical studies which evaluated the relationship between oxidative stress and the myocardial dysfunction in sepsis

Reactive Species

Conclusion

Findings

Conflicts of Interest