scholarly journals Oxidative Stress and Hepatic Monooxygenase Function in Coronary Heart Disease Patients with Multiple Organ Dysfunction

2008 ◽  
Vol 4 (4) ◽  
pp. 32
Author(s):  
V. A. Nepomnyashchikh ◽  
V. V. Lomivorotov ◽  
M. N. Deryagin ◽  
V. N. Lomivorotov ◽  
L. G. Knyazkova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Hepatic Monooxygenase

scholarly journals Sepsis, mitochondrial failure and multiple organ dysfunction

2014 ◽  
Vol 37 (2) ◽  
pp. 58 ◽  
Author(s):  
Josefina Duran-Bedolla ◽  
Marco A Montes de Oca-Sandoval ◽  
Vianey Saldaña-Navor ◽  
José A Villalobos-Silva ◽  
Maria Carmen Rodriguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Physiological State ◽  
Redox Balance ◽  
Multiple Organ ◽  
Reactive Species ◽  
Systemic Inflammatory Response ◽  
Antioxidant Systems ◽  
Multiple Organ Dysfunction

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.

scholarly journals Cardiovascular Insufficiency, Abdominal Sepsis, and Patients’ Age Are Associated with Decreased Paraoxonase-1 (PON1) Activity in Critically Ill Patients with Multiple Organ Dysfunction Syndrome (MODS)

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Iwona Bednarz-Misa ◽  
Magdalena Mierzchala-Pasierb ◽  
Patrycja Lesnik ◽  
Sylwia Placzkowska ◽  
Krzysztof Kedzior ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Septic Shock ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Multiple Organ Dysfunction ◽  
Infection Site ◽  
A Site

Oxidative stress and uncontrolled inflammation are hallmarks of sepsis, leading to organ failure and death. As demonstrated in animal studies, oxidative stress can be alleviated by antioxidant therapies. Paraoxonase-1 (PON1) is a serum-based antioxidant, anti-inflammatory agent, detoxifier, and quorum-sensing factor found to be a prognostic marker in sepsis. However, its associations with multiple organ dysfunction syndrome (MODS), a complication of sepsis and the leading cause of death in the surgical intensive care units (ICU), as well as with specific organ dysfunction, infection site, and invading pathogen remain unknown. Therefore, we measured arylesterase activity of PON1 in 87 individuals (35 with MODS) and related it to the clinical type, organ failure, infection site, pathogens, and hematological and biochemical indices of inflammation at admission to ICU and during a five-day follow-up. Suitability of PON1 and its indices derived from a follow-up as biomarkers in MODS was evaluated as well. MODS was associated with decreased PON1, more so in patients with septic shock, displaying an excellent accuracy as a marker of MODS (91%) and a fair one as a marker in differentiating septic shock from severe sepsis (76%). Decreased admission PON1 accompanied cardiovascular insufficiency (CVI), and, as its marker, PON1 displayed a good accuracy (82%). It was also associated with the abdomen as a site of infection but not with an invading pathogen. In multivariate analysis, 50% of variability in PON1 activity in patients with MODS was explained by the patients’ age, CVI, and abdomen as a site of infection. Patients with septic shock, CVI, and abdominal MODS had distinctly different dynamics of PON1 during a follow-up. Mean PON1 activity during the follow-up reflected the associations observed for admission PON1 but was also significantly associated with metabolic dysfunction. Our results show PON1 potential as a biomarker in MODS, particularly as an indicator of CVI.

scholarly journals Klotho deficiency aggravates sepsis-related multiple organ dysfunction

2019 ◽  
Vol 316 (3) ◽  
pp. F438-F448 ◽  
Author(s):  
Lectícia B. Jorge ◽  
Fernanda O. Coelho ◽  
Talita R. Sanches ◽  
Denise M. A. C. Malheiros ◽  
Leandro Ezaquiel de Souza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Organ Dysfunction ◽  
Ischemia Reperfusion Injury ◽  
Blood Pressure Response ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Cecal Ligation ◽  
Kidney Tissue ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

Sepsis-induced organ failure is characterized by a massive inflammatory response and oxidative stress. Acute kidney injury (AKI) occurs in approximately half of patients in septic shock, and the mortality associated with sepsis-induced AKI is unacceptably high. Klotho is a protein expressed by renal cells and has anti-senescence properties. Klotho has also been shown to protect the kidneys in ischemia-reperfusion injury and to have antioxidant properties. To analyze the role of Klotho in sepsis-related organ dysfunction and AKI, we used a cecal ligation and puncture (CLP) model of sepsis in heterozygous Klotho-haploinsufficient mice and their wild-type littermates (CLP- Kl/+ and CLP-WT mice, respectively). In comparison with the CLP-WT mice, CLP- Kl/+ mice showed lower survival, impaired renal function, impaired hepatic function, greater oxidative stress, upregulation of inflammatory pathways (at the systemic and kidney tissue levels), and increased NF-κB activation. It is noteworthy that CLP- Kl/+ mice also showed lower heart-rate variability, less sympathetic activity, impaired baroreflex sensitivity to sodium nitroprusside, and a blunted blood pressure response to phenylephrine. We also demonstrated that sepsis creates a state of acute Klotho deficiency. Given that low Klotho expression exacerbates sepsis and multiple organ dysfunction, Klotho might play a protective role in sepsis, especially in elderly individuals in whom Klotho expression is naturally reduced.

Development of oxidative stress in blood of patients with severe polytrauma before and after development of multiple organ dysfunction syndrome

2008 ◽  
Vol 21 (2) ◽  
pp. 267-270
Author(s):  
Myroslav Stupnytskyi ◽  
Nadiya Fartushok ◽  
Yuriy Fedevych ◽  
Olga Melekh ◽  
Galina Kashaeva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Before And After

Disseminated intravascular coagulation in meningococcal sepsis

2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin
Keyword(s):  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Skin Necrosis ◽  
Multiple Organ ◽  
Meningococcal Sepsis ◽  
Multiple Organ Dysfunction ◽  
Intravascular Coagulation ◽  
Therapeutic Concepts ◽  
New Therapeutic Concepts ◽  
Coagulation And Fibrinolysis

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.

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