Increased hepatic amino nitrogen conversion after elective cholecystectomy in man

Abstract

1. The effect of elective, uncomplicated cholecystectomy on plasma clearances of amino acids and on amino acid-stimulated urea synthesis was investigated in 10 patients, pre-operatively and on the first post-operative day, and compared with six controls treated identically apart from the surgery. 2. A mixture of amino acids was given as a prime-continuous infusion. Steady-state concentrations 75% higher than basal were attained and were maintained for 90 min. The clearances of amino acids were calculated as the ratios between amino acid infusion rate and the concentration. The urea synthesis rate was calculated as urinary excretion corrected for accumulation and intestinal loss. 3. After surgery the fasting plasma concentrations of alanine, arginine, glutamine plus glutamate, glycine, proline, lysine and threonine decreased by 20–30%, but were unchanged in the control group. The plasma clearance of α-amino nitrogen increased from 5.1 ± 1.2 ml/s before surgery (mean ± sd) to 6.1 ± 1.1 ml/s (P < 0.05, paired t-test) after surgery due to increased clearances of the above-mentioned amino acids. In the control group, the clearance decreased from 6.4 ± 1.6 to 5.9 ± 1.1 (P < 0.05, paired t-test). The amino acid-stimulated urea synthesis rate after surgery was 37 ± 9 μmol of N/s vs 30 ± 6 (P < 0.01, paired t-test) in the controls despite a lower α-amino nitrogen concentration (4.5 ± 0.5 mmol/l vs 5.1 ± 0.5 mmol/l, P < 0.05, paired t-test). The post-operative urea synthesis rate exceeded the amino nitrogen infusion by 20%. 4. Post-operatively, the insulin response to the amino acid infusion more than doubled, and the glucagon response increased by 54 %. Fasting Cortisol doubled but decreased similarly to controls during amino acid infusion. 5. After surgery amino nitrogen was cleared from the plasma pool by the liver more rapidly than it was released into the pool. 6. Our data indicate that the liver is partly responsible for the post-operative catabolism. This is not attributable to increased substrate load on the liver, but results from changed hepatic kinetics of amino nitrogen conversion. The altered hormonal responses may play a role in this condition.