Hepatic insufficiency and increased proteolysis, cardiac output, and oxygen consumption following hemorrhage

Circ Shock. 1991 Oct;35(2):78-86.

Abstract

Thirty dogs underwent hemorrhage over a 60-min period to a predetermined O2 debt of 60-120 mL O2/kg, monitored with a Beckman metabolic cart, and then were resuscitated with 120% of the shed volume. Twenty survived and were followed over the next 7 days. On day 4, hepatic insufficiency was suggested by an elevation in [total amino acids] and [lactate] and a decrease in [urea] and [branched-chain amino acids]/[aromatic amino acids]. Net whole body catabolism on day 4 is suggested by a decrease in [glutamine] and an increase in plasma [3-methylhistidine], [phenylalanine], and [tyrosine]. These changes were significantly related to cardiac index, mean blood pressure, [lactate], O2 debt, and shed volume during the hemorrhage 4 days earlier. On day 7 there was a significant increase in the cardiac index and the VO2. These data suggest that hemorrhage induces sequelae similar to major injury or sepsis: hepatic insufficiency, net catabolism, hypermetabolism, and a hyperdynamic circulation. The hyperdynamic circulation may be necessary to meet increased tissue delivery requirements for O2 and amino acids.

MeSH terms

  • Amino Acids / blood
  • Amino Acids, Branched-Chain / blood
  • Animals
  • Blood Glucose / metabolism
  • Cardiac Output*
  • Dogs
  • Endopeptidases / metabolism*
  • Glutamine / blood
  • Hemodynamics
  • Hemorrhage / physiopathology*
  • Lactates / blood
  • Lactic Acid
  • Liver / physiopathology*
  • Methylhistidines / blood
  • Oxygen Consumption*
  • Urea / blood

Substances

  • Amino Acids
  • Amino Acids, Branched-Chain
  • Blood Glucose
  • Lactates
  • Methylhistidines
  • Glutamine
  • Lactic Acid
  • Urea
  • Endopeptidases
  • 3-methylhistidine