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Complement, granulocytes, and shock lung.

P R Craddock

    The American Journal of Emergency Medicine
    |January 1, 1984
    PubMed
    Summary

    Complement activation during hemodialysis causes lung leukostasis, leading to shock lung. This process is mediated by C5a-desarg and is self-limiting due to receptor downregulation.

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    Area of Science:

    • Pulmonary Medicine
    • Immunology
    • Nephrology

    Background:

    • Intravascular leukostasis in pulmonary microvasculature is a key finding in shock lung.
    • Similar leukostasis occurs during hemodialysis, linked to complement activation by cellophane dialyzers.

    Purpose of the Study:

    • To investigate the mechanism of complement-mediated leukostasis and its role in shock lung.
    • To explore the correlation between C5a-desarg levels and shock lung onset.

    Main Methods:

    • Observational study analyzing histologic findings in shock lung patients and hemodialysis patients.
    • In vitro studies to assess endothelial damage mediated by granulocytes.
    • Plasma C5a-desarg level measurements correlated with clinical outcomes.

    Main Results:

    • Cellophane dialyzers trigger complement activation, generating C5a-desarg, which causes granulocyte aggregation and pulmonary microvascular occlusion.
    • Endothelial damage is suggested to be mediated by hydrogen peroxide from adherent granulocytes.
    • A strong correlation exists between plasma C5a-desarg and shock lung onset post-trauma, burns, or sepsis.

    Conclusions:

    • C5a-desarg-mediated pulmonary leukostasis is a significant factor in shock lung development.
    • The process is self-limiting due to granulocyte receptor downregulation, mitigating lung damage.

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