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Protein and fat utilization in shock.

A M Daniel, C H Pierce, H M Shizgal

    Surgery
    |November 1, 1978
    PubMed
    Summary
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    In shock, dogs showed reduced free fatty acid oxidation, indicating a metabolic shift. Protein oxidation increased to compensate, highlighting altered energy substrate utilization during critical illness.

    Area of Science:

    • Cardiovascular Physiology
    • Metabolic Biochemistry
    • Critical Care Medicine

    Background:

    • Previous research indicated shock increases substrate oxidation via lactate/pyruvate pathways.
    • This implies a potential decrease in free fatty acid (FFA) oxidation during shock.

    Purpose of the Study:

    • To investigate FFA metabolism in dogs experiencing shock.
    • To test the hypothesis that FFA oxidation decreases during shock.

    Main Methods:

    • Infusion of carbon-14 labeled fatty acid in normal dogs and dogs in cardiac tamponade or endotoxin shock.
    • Measurement of arterial fatty acid concentration, FFA turnover, FFA oxidation rate, and CO2 production.

    Main Results:

    • Shock significantly decreased arterial FFA concentration and FFA turnover (p < 0.05).

    Related Experiment Videos

  • The rate and percentage of CO2 derived from FFA oxidation were significantly reduced in shock (p < 0.05).
  • Urea production increased, and protein oxidation contribution to CO2 rose from 23% to 50% in shock.

    • Conclusions:

    • Shock significantly impairs free fatty acid metabolism and oxidation in dogs.
    • Energy metabolism shifts towards protein oxidation during shock states.
    • Findings support the hypothesis of decreased FFA utilization and increased protein catabolism in shock.