To examine alterations in
amino acid metabolism after
trauma and
sepsis, male Sprague-Dawley rats underwent no operation (control, CON), celiotomy (
trauma, TRA), or cecal
ligation and
puncture (
sepsis, CLP). After 16 hr, plasma
amino acid concentrations were determined. A second group of similarly prepared animals underwent isolated liver perfusion, and net
amino acid uptake or release was determined over 30 min.
Sepsis significantly decreased total
amino acid concentration in portal plasma (CON, 3486 +/- 156 nmole/ml; TRA, 3407 +/- 150 nmole/ml; CLP, 2738 +/- 148 nmole/ml).
Glutamine concentrations were uniformly lower in portal plasma than in arterial plasma in all states. There were depressed concentrations of the
branched chain amino acids (BCAA) in portal plasma after
trauma but not
sepsis. In the isolated liver perfusion model, a marked increase in
amino acid uptake was induced by
sepsis (CON, 39.9 +/- 7.9 mumol/g liver
protein; TRA, 49.5 +/- 17.3 mumol/g liver
protein; CLP, 124 +/- 11 mumol/g liver
protein). In addition, there was significantly greater uptake of
threonine,
asparagine,
proline,
methionine,
tyrosine, and
arginine. Although the BCAA
isoleucine and
valine were taken up to a greater extent in
sepsis, the overall BCAA uptake was not significantly greater in
sepsis than in control (CON 6.92 +/- 2.15 mumol/g liver
protein vs CLP 15.8 +/- 1.9 mumol/g liver
protein). The greatest increase in uptake following
sepsis was among the gluconeogenic precursor
amino acids alanine,
glycine,
threonine, and
serine (CON, 27.0 +/- 4.2 mumol/g liver
protein, TRA, 38.8 +/- 8.9 mumol/g liver
protein; CLP, 62.8 +/- 6.0 mumol/g liver
protein).(ABSTRACT TRUNCATED AT 250 WORDS)