title: Change in brain glucose after enteral nutrition in subarachnoid hemorrhage.
abstract: BACKGROUND
  The alteration of brain extracellular glucose after enteral nutrition (EN) remains unclear. In this study, we used brain microdialysis methods to estimate whether the physiologic elevation of plasma glucose following EN affects brain glucose metabolism of aneurysmal subarachnoid hemorrhage (SAH) patients.
  
  
  METHODS
  Brain extracellular glucose, lactate, glycerol, glutamate, and pyruvate were measured with a brain microdialysis probe in 12 patients (mean age: 60.0 y+/-7.8 y) after SAH. The EN was initially administered a mean of 3.2 d after the onset of SAH. All of the measured parameters were estimated before and after EN.
  
  
  RESULTS
  Cerebral perfusion pressure did not significantly change after SAH during the study period. Plasma glucose rose significantly after EN (141.4+/-11.6mg/dL before EN versus 183.8+/-26.2mg/dL immediately after EN (P=0.0006), 177.7+/-30.2mg/dL at 2h after EN (P=0.0033)). The brain extracellular glucose before EN (2.5+/-0.92mmol/L) was significantly lower than the levels measured just after (3.49+/-1.0mmol/L, P=0.0186) and 2h after the end of EN (3.70+/-1.0mmol/L, P=0.0053). Brain extracellular concentrations of lactate, glutamate, pyruvate, and glycerol showed no significant changes.
  
  
  CONCLUSIONS
  Brain extracellular glucose increased after the transient elevation of plasma glucose following EN. These results suggest that brief, physiologic elevations in plasma glucose after EN produced no changes in brain extracellular glutamate concentration or lactate/pyruvate ratio. These data may help determine the plasma glucose levels most effective for avoiding brain metabolic acidosis in patients after SAH. It remains unclear, however, how SAH itself influences these findings.
authors.affiliation: Division of Emergency and Critical Care Medicine, Department of Acute Medicine, Nihon University School of Medicine, Itabashi, Tokyo. kosaku@med.nihon-u.ac.jp
authors.forename: Kosaku
authors.initials: K
authors.lastname: Kinoshita
authors.forename: Takashi
authors.initials: T
authors.lastname: Moriya
authors.forename: Akira
authors.initials: A
authors.lastname: Utagawa
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sakurai
authors.forename: Takeo
authors.initials: T
authors.lastname: Mukoyama
authors.forename: Makoto
authors.initials: M
authors.lastname: Furukawa
authors.forename: Junko
authors.initials: J
authors.lastname: Yamaguchi
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Tanjoh
mesh_terms: D000368:Aged; D001783:Blood Flow Velocity; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001921:Brain / Q000378:metabolism*; D004750:Enteral Nutrition; D005947:Glucose / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D002532:Intracranial Aneurysm / Q000097:blood / Q000378:metabolism / Q000628:therapy*; D007427:Intracranial Pressure; D007773:Lactates / Q000378:metabolism; D017551:Microdialysis / Q000379:methods; D008875:Middle Aged; D019289:Pyruvic Acid / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000378:metabolism / Q000628:therapy*
chemical_list: D001786:Blood Glucose; D007773:Lactates; D018698:Glutamic Acid; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol