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Ammonium chloride and α‐ketoglutaric acid increase glutamine availability in the early phase of induced acute metabolic acidosis
Author(s) -
Nordgren A.,
Karlsson T.,
Wiklund L.
Publication year - 2006
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2006.01071.x
Subject(s) - glutamine , medicine , isotonic saline , acidosis , endocrinology , metabolism , ammonium , metabolic acidosis , ammonium chloride , biochemistry , chemistry , amino acid , organic chemistry
Background: Glutamine deficiency in critical illness is associated with increased morbidity and mortality. We hypothesized that ammonium chloride (NH 4 Cl) and α‐ketoglutaric acid (α‐KGA) infusions could increase glutamine availability possibly through de novo synthesis in the liver. Methods: Anesthetized post‐absorptive pigs were allocated to four groups ( n = 8). The study groups received either a 4‐h intravenous infusion of α‐KGA, 11.4 μmol/kg/min and NH 4 + , 9.7 μmol/kg/min (group 1), or α‐KGA, 2.85 μmol/kg/min and NH 4 + , 46.3 μmol/kg/min (group 2), or α‐KGA, 11.4 μmol/kg/min (group 3), or isotonic saline (control group). Plasma concentrations of glutamine and glutamine exchange in liver, intestine and skeletal muscle were investigated. Results: Plasma glutamine concentrations in group 1 (58% increase) were greater ( P < 0.05) compared with the control group (14% decrease) and group 3 (13% decrease), and in group 2 (91% increase) compared with the control group, group 3 ( P < 0.0001) and group 1 ( P < 0.05). Intestinal glutamine extractions in group 2 were significantly greater ( P < 0.01) compared with all other groups. Neither the liver nor the hind leg increased its release of glutamine. Arterial pH decreased (all P < 0.001) to 7.39 ± 0.01 in the control group, 7.30 ± 0.01 in group 1, 7.19 ± 0.01 in group 2 and 7.35 ± 0.01 in group 3. Conclusion: Infusions of α‐KGA and NH 4 Cl, to a pH range of 7.20–7.30, did not enhance hind leg or hepatic glutamine release. The increased plasma concentrations of glutamine were effects of NH 4 Cl, not α‐KGA, and caused either by de novo synthesis or decreased degradation.