Hypermetabolism and increased peripheral release of amino acids after subarachnoidal hemorrhage and its operative treatment

The metabolic response to surgery for acute subarachnoidal hemorrhage and its modification by amino acid infusions was studied. Thirty patients with acute subarachnoidal hemorrhage were randomly assigned to receive for 12 h either an infusion of glucose and a balanced amino acid solution (1.68 MJ = 400 kcal/d and 0.15 gN · kg−1 · d−1; group AA) or a glucose and a solution containing 20% of total nitrogen as alanyl-glutamine (1.68 MJ = 400 kcal/d and 0.15 gN · kg−1 · d−1; group ALAGLN). A separate control group received glucose alone (1.68 MJ = 400 kcal/d). The infusions started 12 h after operation. All patients received corticosteroids. Despite a higher arterial glutamine concentration in the ALAGLN-group (791 ± 195 μmol/L vs. AA 581 ± 112 μmol/L, and control 571 ± 82 μmol/L; p < 0.05) the net release of glutamine from the leg was similar in all groups (ALAGLN: 39 ± 47 μmol/min, AA: 26 ± 18 μmol/min, and control: 24 ± μmol/min, NS). Also the release of alanine (ALAGLN: 35 ± 24 μmol/min, AA: 34 ± 24 μmol/min, and control: 30 ± 18 μmol/min) and total amino acids (ALAGLN: 133 ± 131 μmol/min, AA: 125 ± 98 μmo/min, and control: 112 ± 72 μmol/min) were similar in all groups. All groups were characterized by a pattern of preoperative hypermetabolism that persisted after the operation. The hypermetabolism was not related to increased peripheral oxygen consumption, since femoral oxygen consumption (VO2) represented only 3% of the whole body VO2.