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Related Experiment Videos

Plasma fibronectin and complement activation in coronary bypass surgery.

S J Chadwick, R D Stanbridge, J F Mowbray

    The British Journal of Surgery
    |September 1, 1986
    PubMed
    Summary

    Complement activation during cardiopulmonary bypass does not significantly reduce plasma fibronectin levels. This suggests sepsis, not complement activation alone, causes fibronectin reduction in severe sepsis patients.

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    Area of Science:

    • Biochemistry
    • Immunology
    • Cardiovascular Surgery

    Background:

    • Severe sepsis is associated with reduced plasma fibronectin and activated complement.
    • The interaction between complement activation and plasma fibronectin levels remains unclear.
    • Cardiopulmonary bypass is known to activate the complement system.

    Purpose of the Study:

    • To investigate the effect of complement activation on plasma fibronectin concentrations.
    • To determine if complement activation, independent of sepsis, influences fibronectin levels.
    • To utilize cardiopulmonary bypass as a model for studying complement activation.

    Main Methods:

    • Plasma fibronectin, hematocrit, C3, and C5 levels were measured during cardiopulmonary bypass.
    • Neutrophil counts were monitored during the procedure.

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  • Changes in these parameters were analyzed to assess complement activation and its impact on fibronectin.

    • Main Results:

    • After 15 minutes of bypass, plasma fibronectin and hematocrit showed similar percentage changes.
    • Complement components C3 and C5 demonstrated significantly greater changes than hematocrit, indicating complement consumption.
    • A significant increase in neutrophil count was observed during the first 60 minutes of bypass, consistent with complement activation.

    Conclusions:

    • Complement activation during cardiopulmonary bypass does not appear to significantly reduce plasma fibronectin concentrations.
    • The reduction of plasma fibronectin observed in severe sepsis is unlikely to be solely due to complement activation.
    • Further research is needed to elucidate the precise mechanisms underlying fibronectin reduction in sepsis.