Effect of injury and infection on visceral metabolism and circulation.
To characterize the role of the liver and kidney in the metabolic response to injury and infection, selective catheterization of the hepatic (42 veins) and renal veins (21 veins) was performed in 31 burn patients (mean burn size: 51% TBS), studied 4-129 days postinjury. Blood flow was determined by standard clearance techniques (ICG and PAH), and simultaneous arterial and hepatic and/or renal vein blood was obtained for oxygen, glucose, lactate, pyruvate, and amino acids. Patients studied in the first to third weeks postinjury were classified as noninfected (8 studies), bacteremic (8 studies), or bacteremic with complications (5 studies). There was no difference in age, weight, mean burn size, pulse rate, blood pressure, rectal temperature, total body oxygen consumption, or cardiac index among these groups. Estimated hepatic blood flow (EHBF) and hepatic substrate balance of these patients were compared with postabsorptive normal subjects in the literature (mean +/- SEM or range). :Formula: (See Text) Thermal injury alone resulted in marked increases in EHBF, hepatic oxygen uptake, and glucogenesis. The added insult of bacteremia significantly increased hepatic glucose output; as clinical sepsis progressed, glucose output decreased sharply. The kidney consistently demonstrated a net uptake of glucose in all studies. The changes in hepatic glucose output in bacteremic patients occurred without significant differences in EHBF, oxygen utilization or lactate uptake, but were associated with marked alterations in amino acid uptake.
D000328:Adult; D000596:Amino Acids / Q000378:metabolism; D002056:Burns / Q000150:complications / Q000378:metabolism*; D005260:Female; D005943:Gluconeogenesis; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation; D008297:Male; D010101:Oxygen Consumption; D018805:Sepsis / Q000150:complications / Q000378:metabolism*
D000596:Amino Acids