Inflammation, endothelium, and coagulation in sepsis

Schouten, Marcel; Wiersinga, W. Joost; Levi, Marcel; Poll, Tom van der

doi:10.1189/jlb.0607373

Cited by 566 publications

(523 citation statements)

References 124 publications

(125 reference statements)

Supporting

Mentioning

485

Contrasting

Unclassified

Order By: Relevance

“…2008). In most severe cases, when the hypotension is not resuscitated with crystalloid solution perfusion, the illness provokes a septic shock, which generally leads to death.…”

Section: Introductionmentioning

confidence: 99%

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

et al. 2017

View full text Add to dashboard Cite

If it is sustained for several days, sepsis can trigger severe abnormalities of cardiac function which leads to death in 50% of cases. This probably occurs through activation of toll‐like receptor‐9 by bacterial lipopolysaccharides and overproduction of proinflammatory cytokines such as TNF‐α and IL‐1β. In contrast, early sepsis is characterized by the development of tachycardia. This study aimed at determining the early changes in the cardiac function during sepsis and at finding the mechanism responsible for the observed changes. Sixty male Wistar rats were randomly assigned to two groups, the first one being made septic by cecal ligation and puncture (sepsis group) and the second one being subjected to the same surgery without cecal ligation and puncture (sham‐operated group). The cardiac function was assessed in vivo and ex vivo in standard conditions. Several parameters involved in the oxidative stress and inflammation were determined in the plasma and heart. As evidenced by the plasma level of TNF‐α and gene expression of IL‐1β and TNF‐α in the heart, inflammation was developed in the sepsis group. The cardiac function was also slightly stimulated by sepsis in the in vivo and ex vivo situations. This was associated with unchanged levels of oxidative stress, but several parameters indicated a lower cardiac production of reactive oxygen species in the septic group. In conclusion, despite the development of inflammation, early sepsis did not increase reactive oxygen species production and did not reduce myocardial function. The depressant effect of TNF‐α and IL‐1β on the cardiac function is known to occur at very high concentrations. The influence of low‐ to moderate‐grade inflammation on the myocardial mechanical behavior must thus be revisited.

show abstract

“…2008). In most severe cases, when the hypotension is not resuscitated with crystalloid solution perfusion, the illness provokes a septic shock, which generally leads to death.…”

Section: Introductionmentioning

confidence: 99%

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Although several aspects of inflammation were studied in the in vitro model, it has substantial inherent limitations. Important cell systems like endothel, which is known to be an important part of the inflammatory network in sepsis (170), and the solid organs are of course missing. The blood was incubated in plastic tubes, and was thereby in constant contact with an artificial surface during incubation.…”

Section: Pig In Vitro Serum and Whole Blood Modelsmentioning

confidence: 99%

Candidate inhibitors of porcine complement

Thorgersen¹,

Ghebremariam²,

Thurman³

et al. 2007

Molecular Immunology

View full text Add to dashboard Cite

“…It is de ned as systolic blood pressure (SBP) <90 mmHg, mean arterial pressure (MAP) <70 mmHg, or a decrease in SBP of >40 mmHg in adults or less than two standard deviation below normal according to age, despite adequate uid resuscitation [3,4] (Hemodynamic variables, Table 1). Septic shock can be understood as severe sepsis with cardiovascular failure.…”

Section: Current Concepts In Sepsismentioning

confidence: 99%

Sepsis, mitochondrial failure and multiple organ dysfunction

Dúran-Bedolla

Oca-Sandoval²,

Saldaña-Navor³

et al. 2014

CIM

View full text Add to dashboard Cite

Purpose: e 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 ndings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated in ammatory response. Involved in the pathogenesis of sepsis are the activation of in ammatory, 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. e 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 in ammatory response.e loss of the redox balance, together with a systemic in ammatory 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 e ective therapies and better prognosis for patients with sepsis and organ dysfunction.

show abstract

Inflammation, endothelium, and coagulation in sepsis

Cited by 566 publications

References 124 publications

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

Candidate inhibitors of porcine complement

Sepsis, mitochondrial failure and multiple organ dysfunction

Contact Info

Product

Resources

About