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Oxidant-mediated, CD18-dependent microvascular dysfunction induced by complement-activated granulocytes.

D L Carden1, J K Smith, R J Korthuis

  • 1Department of Physiology, Louisiana State University Medical Center, School of Medicine, Shreveport 71130.

The American Journal of Physiology
|April 1, 1991
PubMed
Summary
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Complement-activated granulocytes cause microvascular dysfunction in skeletal muscle. Neutrophil depletion and adherence inhibition prevent this, but xanthine oxidase does not.

Area of Science:

  • Physiology
  • Immunology
  • Vascular Biology

Background:

  • Complement activation leads to granulocyte recruitment and microvascular dysfunction.
  • Neutrophil adherence plays a critical role in inflammatory processes.
  • Skeletal muscle microvasculature is susceptible to inflammatory damage.

Purpose of the Study:

  • To elucidate the mechanisms by which complement-activated granulocytes induce microvascular dysfunction in skeletal muscle.
  • To investigate the role of neutrophil adherence and reactive oxygen species in ZAP-induced microvascular permeability.

Main Methods:

  • Assessment of microvascular permeability using the solvent drag reflection coefficient (sigma) in canine gracilis muscle.
  • Measurement of neutrophil infiltration via myeloperoxidase activity.

Related Experiment Videos

  • Intervention with antineutrophil serum (ANS), IB4 antibody, xanthine oxidase inhibitors, deferoxamine, and catalase.

    • Main Results:

    • Zymosan-activated plasma (ZAP) significantly increased vascular permeability (sigma = 0.51).
    • Neutropenia (ANS) and inhibition of neutrophil adherence (IB4) normalized ZAP-induced permeability (sigma ≈ 0.9).
    • Deferoxamine and catalase also reduced ZAP-induced permeability, while xanthine oxidase inhibition did not.

    Conclusions:

    • Complement-induced microvascular dysfunction in skeletal muscle is primarily mediated by granulocyte infiltration and adherence.
    • Inhibition of neutrophil adherence is a key therapeutic target for mitigating ZAP-induced microvascular injury.
    • The role of xanthine oxidase in this specific model of microvascular dysfunction appears limited.