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. Copyright 2010 Elsevier Inc. All rights reserved.
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. Copyright 2010 Elsevier Inc. All rights reserved.
Authors: J Michael Schmidt; Jan Claassen; Sang-Bae Ko; Hector Lantigua; Mary Presciutti; Kiwon Lee; E Sander Connolly; Stephan A Mayer; David S Seres; Neeraj Badjatia Journal: Crit Care Date: 2012-01-25 Impact factor: 9.097
Authors: Peter J Hutchinson; Ibrahim Jalloh; Adel Helmy; Keri L H Carpenter; Elham Rostami; Bo-Michael Bellander; Martyn G Boutelle; Jeff W Chen; Jan Claassen; Claire Dahyot-Fizelier; Per Enblad; Clare N Gallagher; Raimund Helbok; Lars Hillered; Peter D Le Roux; Sandra Magnoni; Halinder S Mangat; David K Menon; Carl-Henrik Nordström; Kristine H O'Phelan; Mauro Oddo; Jon Perez Barcena; Claudia Robertson; Elisabeth Ronne-Engström; Juan Sahuquillo; Martin Smith; Nino Stocchetti; Antonio Belli; T Adrian Carpenter; Jonathan P Coles; Marek Czosnyka; Nil Dizdar; J Clay Goodman; Arun K Gupta; Troels H Nielsen; Niklas Marklund; Ambroise Montcriol; Mark T O'Connell; Maria A Poca; Asita Sarrafzadeh; Richard J Shannon; Jane Skjøth-Rasmussen; Peter Smielewski; John F Stover; Ivan Timofeev; Paul Vespa; Elizabeth Zavala; Urban Ungerstedt Journal: Intensive Care Med Date: 2015-09 Impact factor: 17.440