title: Glutamate-containing parenteral nutrition doubles plasma glutamate: a risk factor in neurosurgical patients with blood-brain barrier damage?
abstract: OBJECTIVE
  Animal studies have shown that the elevation of plasma glutamate levels increase cerebral edema formation whenever the blood-brain barrier is disturbed. Therefore, changes in plasma glutamate levels as influenced by the administration of a glutamate-containing amino acid solution were investigated in neurosurgical patients.
  
  
  METHODS
  Prospective, descriptive study.
  
  
  METHODS
  Eight-bed neurosurgical intensive care unit in a university hospital.
  
  
  METHODS
  Twenty-three neurosurgical patients requiring parenteral nutrition.
  
  
  METHODS
  Parenteral nutrition was begun 24 hrs after craniotomy. Patients receiving a glutamate-containing amino acid solution (3.75 g/L glutamate) were compared with patients infused with a glutamate-free solution.
  
  
  RESULTS
  Arterial plasma and urine amino acids were analyzed using high-performance liquid chromatography. Administration of a glutamate-containing solution doubled plasma glutamate levels in neurosurgical patients (from 53.3 +/- 9.8 microM [preinfusion] to 98.5 +/- 18.7 microM [after 4 hrs of infusion]; p < 0.001), whereas no elevation was seen when infusing a glutamate-free solution (from 52.3 +/- 7.3 [1 hr of infusion] to 53.6 +/- 6.4 microM [4 hrs of infusion]). Upon terminating the glutamate-containing infusion, arterial plasma glutamate levels decreased immediately (from 120 +/- 13.2 microM to 81.2 +/- 19.5 microM). Glutamate as infused in excess appears to exceed a renal threshold and is eliminated renally.
  
  
  CONCLUSIONS
  As shown in animal models, administration of a glutamate-containing amino acid solution significantly increased plasma glutamate levels. Because such an increase in plasma glutamate levels could aggravate cerebral edema formation, glutamate-containing amino acid solutions cannot be recommended for patients with a disturbed blood-brain barrier.
authors.affiliation: Institute for Neurosurgical Pathophysiology, Johannes Gutenberg University, Mainz, Germany.
authors.forename: J F
authors.initials: JF
authors.lastname: Stover
authors.forename: O S
authors.initials: OS
authors.lastname: Kempski
mesh_terms: D001216:Asparagine / Q000097:blood / Q000652:urine; D001224:Aspartic Acid / Q000097:blood / Q000652:urine; D001812:Blood-Brain Barrier / Q000187:drug effects; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D002851:Chromatography, High Pressure Liquid; D003399:Craniotomy / Q000009:adverse effects*; D005260:Female; D018698:Glutamic Acid / Q000008:administration & dosage* / Q000097:blood* / Q000652:urine; D005973:Glutamine / Q000097:blood / Q000652:urine; D006785:Hospitals, University; D006801:Humans; D007362:Intensive Care Units; D008297:Male; D008875:Middle Aged; D010288:Parenteral Nutrition; D011446:Prospective Studies; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D005973:Glutamine; D001224:Aspartic Acid; D018698:Glutamic Acid; D001216:Asparagine