HYPERMETABOLISM AND INCREASED PERIPHERAL RELEASE OF AMINO-ACIDS AFTERSUBARACHNOID HEMORRHAGE AND ITS OPERATIVE TREATMENT

The metabolic response to surgery for acute subarachnoidal hemorrhage and its modification by amino acid infusions was studied. Thirty patie nts with acute subarachnoidal hemorrhage were randomly assigned to rec eive 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 AL AGLN). A separate control group received glucose alone (1.68 MJ = 400 kcal/d). The infusions started 12 h after operation. All patients rece ived corticosteroids. Despite a higher arterial glutamine concentratio n in the ALAGLN-group (791 +/- 195 mu mol/L vs. AA 581 +/- 112 mu mol/ L, and control 571 +/- 82 mu mol/L; p < 0.05) the net release of gluta mine from the leg was similar in all groups (ALAGLN: 39 +/- 47 mu mol/ min, AA: 26 +/- 18 mu mol/min, and control: 24 +/- 14 mu mol/min, NS). Also the release of alanine (ALAGLN: 35 +/- 24 mu mol/min, AA: 34 +/- 24 mu mol/min, and control: 30 +/- 18 mu mol/min) and total amino aci ds (ALAGLN: 133 +/- 131 mu mol/min, AA: 125 +/- 98 mu mol/min, and con trol: 112 +/- 72 mu mol/min) were similar in all groups. All groups we re characterized by a pattern of preoperative hypermetabolism that per sisted after the operation. The hypermetabolism was not related to inc reased peripheral oxygen consumption, since femoral oxygen consumption (VO2) represented only 3% of the whole body VO2.