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Related Experiment Videos

Systemic complement activation and acute lung injury.

G O Till, P A Ward

    Federation Proceedings
    |January 1, 1986
    PubMed
    Summary
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    Complement activation and neutrophils cause acute lung injury in rats. Oxygen-derived free radicals, particularly hydroxyl radical (OH.), produced by neutrophils mediate this microvascular injury.

    Area of Science:

    • Physiology
    • Immunology
    • Pathology

    Background:

    • Intravascular complement activation can lead to acute lung injury.
    • Cobra venom factor (CVF) injection or thermal injury triggers this response in rats.

    Purpose of the Study:

    • To investigate the mechanisms underlying complement-mediated acute lung injury.
    • To identify the role of neutrophils and free radicals in this process.

    Main Methods:

    • Rats were injected with CVF or subjected to thermal injury.
    • Complement and neutrophil levels were manipulated.
    • Interventions included catalase, hydroxyl radical (OH.) scavengers, and iron chelators.

    Main Results:

    • Acute lung injury was characterized by morphological changes and increased vascular permeability.

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  • Complement activation led to neutrophil sequestration in the lungs.
  • Depletion of complement or neutrophils prevented lung injury.
  • Free radical scavengers and iron chelators reduced lung injury.

    • Conclusions:

    • Acute lung injury is dependent on complement activation and neutrophil availability.
    • Neutrophil-derived oxygen-free radicals, especially hydroxyl radical (OH.), are key mediators of acute lung microvascular injury.