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Complement membrane attack complex and hemodynamic changes during human orthotopic liver transplantation.

Mark C Bellamy1, Jacqui A Gedney, Helen Buglass

  • 1Department of Anaesthesia, St James's University Hospital, Leeds, UK. m.c.bellamy@leeds.ac.uk

Liver Transplantation : Official Publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
|February 6, 2004
PubMed
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Complement activation and neutrophil activation occur rapidly during liver transplantation reperfusion, contributing to hemodynamic changes. These findings suggest complement

Area of Science:

  • Immunology
  • Transplantation Medicine
  • Cardiovascular Physiology

Background:

  • Hemodynamic changes and intracellular calcium shifts post-reperfusion in liver transplants are rapid.
  • These changes do not align with cytokine expression timelines.
  • Pre-formed substances, like complement, are postulated to be involved.

Purpose of the Study:

  • To investigate the role of complement activation and neutrophil activation during liver transplantation reperfusion.
  • To correlate complement and neutrophil markers with hemodynamic changes.

Main Methods:

  • Studied 40 adult liver transplant patients.
  • Measured complement components (C3, C4, C3 degradation product, C5b-9 membrane attack complex, CH100) and elastase levels at key time points.

Related Experiment Videos

  • Monitored hemodynamic parameters (cardiac output, systemic vascular resistance) using thermodilution.

    • Main Results:

    • Significant increase in C5b-9 membrane attack complex and C3 degradation product.
    • Significant decrease in C3 and C4 levels.
    • Significant fall in systemic vascular resistance index and increase in cardiac index.
    • Significant rise in elastase levels, indicating neutrophil activation.

    Conclusions:

    • Complement and neutrophil activation occur at reperfusion in liver transplantation.
    • Complement activation, indicated by C5b-9 and C3/C4 consumption, correlates with hemodynamic shifts.
    • Both classical and potentially other complement pathways are involved.
    • These activations may partly explain reperfusion-associated hemodynamic changes.