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 μmole/g liver protein; TRA, 49.5 ± 17.3 μmole/g liver protein; CLP, 124 ± 11 μmole/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 μmole/g liver protein vs CLP 15.8 ± 1.9 μmole/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 μmole/g liver protein, TRA, 38.8 ± 8.9 μmole/g liver protein; CLP, 62.8 ± 6.0 μmol/g liver protein). The results suggest that sepsis significantly alters hepatic amino acid uptake and release, particularly among certain amino acid groups.
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