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Claudia S. Robertson, J. Clay Goodman, Raj K. Narayan, Charles F. Contant, and Robert G. Grossman

ketone bodies may have protective effects. 10, 17 We previously found that, following a severe head injury, cerebral metabolism is almost totally dependent upon the aerobic and anaerobic metabolism of glucose, due to the limited availability of other energy substrates. 25 Because the patients we studied were receiving glucose in their intravenous fluids, it was not possible to know if metabolic changes induced by the head injury per se or by the glucose infusion prevented the mobilization of other substrates in response to fasting. Nor was it possible to determine

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Claudia S. Robertson, Robert G. Grossman, J. Clay Goodman, and Raj K. Narayan

-flow areas being obscured by adjacent areas of hyperemia. In experimental and clinical studies of focal cerebral ischemia, abnormalities of cerebral metabolism persist long after CBF has recovered in tissues that have suffered significant ischemic injury, 10, 17 and regional cerebral metabolic measurements have provided valuable information regarding the severity of the tissue injury in stroke. 1 The purpose of the present study was to determine if two parameters of cerebral metabolism (namely, oxygen consumption and lactate production) could be used to identify the

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Claudia S. Robertson, Raj K. Narayan, Ziya L. Gokaslan, Rajesh Pahwa, Robert G. Grossman, Pedro Caram Jr., and Elizabeth Allen

hypervolemic therapy guided by monitoring pulmonary wedge pressure. Routine medications included phenytoin, morphine for sedation, and antibiotics. Intracranial pressures greater than 20 mm Hg were treated with hyperventilation (pCO 2 25 to 30 mm Hg), cerebrospinal fluid drainage, sedation and paralysis, mannitol, and (if necessary) barbiturates. Because of the marked effect of barbiturates on cerebral metabolism, CBF measurements obtained while patients were in barbiturate coma are not included in this analysis. In the first group of patients, the presence of cerebral

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Michael Sheinberg, Malcolm J. Kanter, Claudia S. Robertson, Charles F. Contant, Raj K. Narayan, and Robert G. Grossman

2 ), end-tidal CO 2 , and SjvO 2 . All parameters were recorded at approximately 1-minute intervals, stored in a computerized data base, plotted against time, and correlated with clinical events and with the intermittent measurements of cerebral blood flow (CBF) and cerebral metabolism. Intermittent Measurements of Cerebral Blood Flow and Metabolism Cerebral blood flow and cerebral metabolic rates of oxygen and lactate were measured every 8 hours. A total of 363 measurements of CBF, or an average of eight measurements per patient (range 1 to 24 per patient

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Daniel F. Kelly, David B. Goodale, John Williams, Daniel L. Herr, E. Thomas Chappell, Michael J. Rosner, Jeff Jacobson, Michael L. Levy, Martin A. Croce, Allen H. Maniker, Gerald J. Fulda, James V. Lovett, Olga Mohan, and Raj K. Narayan

antioxidant. FEBS Lett 357: 83–85, 1995 2. Albanese J , Martin C , Lacarelle B , et al : Pharmacokinetics of long-term propofol infusion used for sedation in ICU patients. Anaesthesiology 73 : 214 – 217 , 1990 Albanese J, Martin C, Lacarelle B, et al: Pharmacokinetics of long-term propofol infusion used for sedation in ICU patients. Anaesthesiology 73: 214–217, 1990 3. Alkire MT , Haier RJ , Barker SJ , et al : Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology 82 : 393 – 403