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Related Concept Videos

Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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Related Experiment Video

Updated: Apr 11, 2026

Assessing Leukocyte-endothelial Interactions Under Flow Conditions in an Ex Vivo Autoperfused Microflow Chamber Assay
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Inflammatory response and extracorporeal circulation.

Florian Kraft1, Christoph Schmidt1, Hugo Van Aken1

  • 1Department of Anaesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster, Münster, Germany.

Best Practice & Research. Clinical Anaesthesiology
|June 11, 2015
PubMed
Summary
This summary is machine-generated.

Cardiac surgery with extracorporeal circulation (EC) triggers inflammation, leading to organ injury. This review explores EC-induced inflammation pathways and therapeutic strategies to mitigate organ dysfunction and improve patient outcomes.

Keywords:
extracorporeal circulationinflammationneutrophil recruitmentsystemic inflammatory response syndrome

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Area of Science:

  • Cardiology
  • Immunology
  • Surgical Science

Background:

  • Cardiac surgery with extracorporeal circulation (EC) often results in a systemic inflammatory response syndrome.
  • Surgical trauma, ischemia-reperfusion injury, and contact with artificial materials activate immune and coagulation pathways.

Purpose of the Study:

  • To review the mechanisms of endothelial cell activation and immune cell recruitment during EC.
  • To discuss the role of reactive oxygen species and nitric oxide in EC-induced organ injury.
  • To examine therapeutic interventions for managing inflammation and multiple organ dysfunction post-EC.

Main Methods:

  • Literature review of pathways involved in systemic inflammatory response syndrome after EC.
  • Analysis of factors contributing to endothelial dysfunction and cellular damage.
  • Evaluation of therapeutic strategies targeting inflammatory pathways.

Main Results:

  • EC activates coagulation, complement, and cellular immune responses, leading to endothelial activation and neutrophil recruitment.
  • Production of reactive oxygen species and nitric oxide contributes to cellular damage and organ injury.
  • Multiple organ dysfunction following EC is linked to increased morbidity and mortality.

Conclusions:

  • Understanding the pathogenesis of EC-induced inflammation is crucial for preventing organ injury.
  • Therapeutic interventions aimed at modulating the inflammatory response can potentially reduce morbidity and mortality after cardiac surgery with EC.