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Abstract

The effect of stress hormones on transsplanchnic balance of basal and infused amino acids (AA: Val, Met, Ile, Leu, Phe, Lys, His) was investigated in healthy men without and with added epinephrine (EPI) and dexamethasone (DEX). Concentrations of AA and blood glucose were measured in arterial and hepatic venous blood before and after primed-continuous (t = 120 minutes) AA infusion without (group I: controls; n = 6, 24 ± 3 years), and with intravenous (IV) EPI infusion (group II: 6 μg/min, t = −75 to 120 minutes; n = 6, 26 ± 5 years) or oral DEX pretreatment (group III: 6 mg/d for 2 days; n = 7, 26 ± 3 years). In the absence of exogenous AA, EPI was demonstrated to increase estimated hepatic plasma flow (EHPF, mL/min: 1,019 ± 133 [mean ± SD] v 737 ± 153; P < .01), splanchnic output of glucose (SGO), and splanchnic uptake of total AA (nmol/kg · min: 4,657 ± 2,014 v 2,802 ± 704; P < .05), of Gln (+78%) and of Gly (+100%). DEX did not affect EHPF or SGO, but doubled basal splanchnic AA uptake (5,446 ± 3,635 nmol/kg · min) and increased that of Gln by 110%. Following AA administration, total splanchnic AA uptake was consistently increased (group I, 8,577 ± 2,380; II, 8,957 ± 3,714; III, 10,757 ± 2,689 nmol/kg · min) as was splanchnic Gln uptake, both of which did not differ versus controls following EPI or DEX exposure. However, metabolic clearance rate (MCR, L/min) of infused AA was elevated by 40% (Met) to 85% (Leu) versus controls in subjects receiving EPI, but unchanged in those receiving oral DEX. These data (1) demonstrate augmented basal splanchnic Gln and total AA uptake after stress hormone exposure; (2) show failure of stress hormones to affect splanchnic uptake of exogenous AA; and (3) provide evidence that EPI, but not DEX, promotes a marked increase in total AA clearance, which potentially may occur in both splanchnic and peripheral tissues.