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Hepatocellular function and nutrient blood flow in experimental peritonitis

R N Garrison, D J Ratcliffe, D E Fry

    Surgery
    |October 1, 1982
    PubMed
    Summary

    Reduced oxygen consumption in peritoneal infection stems from altered nutrient blood flow, not cellular injury. This study investigated hepatic blood flow and mitochondrial function in rats with induced peritonitis.

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    Area of Science:

    • Physiology
    • Pathophysiology
    • Hepatology

    Background:

    • Organ failure and reduced oxygen consumption in peritoneal infection lack a defined pathophysiologic basis.
    • Potential causes include altered tissue nutrient blood flow or primary cellular injury impacting oxygen metabolism.

    Purpose of the Study:

    • To investigate the underlying mechanisms of reduced oxygen consumption during peritoneal infection.
    • To differentiate between altered hepatic blood flow and impaired cellular metabolism as causes of organ dysfunction.

    Main Methods:

    • Peritonitis was induced in rats via cecal ligation and puncture; controls underwent sham operations.
    • Liver mitochondria were isolated to assess oxidative phosphorylation polarographically.
    • Indocyanine green (ICG) clearance was measured at low and high doses to evaluate hepatic blood flow and cellular function.

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    Main Results:

    • Mitochondrial oxidative phosphorylation showed no significant differences between peritonitis and control groups at 6 or 18 hours.
    • At 18 hours post-peritonitis, low-dose ICG clearance (reflecting total hepatic blood flow) was prolonged, indicating reduced blood flow.
    • Extrapolation of ICG clearance data suggested preserved hepatocellular function, as indicated by the intercept at infinite dose.

    Conclusions:

    • Hepatocellular function, assessed by mitochondrial activity and ICG clearance extrapolation, remained intact during peritonitis.
    • Reduced total hepatic blood flow, particularly nutrient blood flow, is identified as the primary cause of decreased oxygen consumption in this model of peritoneal infection.