Document Detail


Cerebral energy failure after subarachnoid hemorrhage: the role of relative hyperglycolysis.
MedLine Citation:
PMID:  17669657     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
After subarachnoid hemorrhage (SAH) cerebral metabolism is significantly impaired. Hyperglycolysis describes the reduction of oxidative metabolism followed by a relative increase of anaerobic glycolysis to maintain energy supply. This phenomenon is known in head injury but has not as yet been shown after SAH. This study was conducted to test the hypothesis that hyperglycolysis is present in SAH patients and is associated with vasospasm. A total of 105 measurements were conducted on 21 SAH patients (age 49+/-15 years, median World Federation of Neurosurgical Societies Grade 4) over the first 5 days following admission. Arteriovenous differences were calculated for oxygen (avDO2) and glucose (avDGlc). Relative hyperglycolysis was defined as metabolic ratio (MR=avDO2[mmol/L]/avDGlc[mmol/L])<3.44. Jugular-venous saturation for oxygen (SjvO2), mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP) were monitored. Relative hyperglycolyis was recorded in 34% of studies after SAH. In hyperglycolytic studies both jugular-venous lactate and SjvO2 were significantly elevated (jugular-venous lactate 14.9+/-9.9 vs. 11.8+/-5.5 mg/dL, p=0.04; SjvO2: 70.0+/-18% vs. 81.7+/-9%, p=0.002). Relative hyperglycolysis is associated with outcome after SAH. In patients who died after SAH almost 50% of studies showed hyperglycolysis, whereas patients who survived without neurological deficit had no hyperglycolytic events. Relative hyperglycolysis is a common event after SAH. It may be associated with relative hyperemia but most importantly with outcome.
Authors:
Matthias F Oertel; Madlen Schwedler; Marco Stein; Dorothee Wachter; Wolfram Scharbrodt; Andrea Schmidinger; Dieter-Karsten Böker
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Publication Detail:
Type:  Journal Article     Date:  2007-07-31
Journal Detail:
Title:  Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia     Volume:  14     ISSN:  0967-5868     ISO Abbreviation:  J Clin Neurosci     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-09-07     Completed Date:  2007-12-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9433352     Medline TA:  J Clin Neurosci     Country:  Scotland    
Other Details:
Languages:  eng     Pagination:  948-54     Citation Subset:  IM    
Affiliation:
Department of Neurosurgery, University Hospital Giessen-Marburg, Klinikstrasse 29, 35385 Giessen, Germany. matthias.oertel@neuro.med.uni-giessen.de
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Pressure / physiology
Brain Diseases, Metabolic / etiology*,  metabolism*,  mortality
Brain Ischemia / etiology*,  metabolism*,  mortality
Cerebral Arteries / physiopathology
Cerebrovascular Circulation / physiology
Cerebrum / blood supply,  metabolism,  physiopathology
Energy Metabolism / physiology
Female
Glucose / metabolism
Glycolysis / physiology*
Humans
Intracranial Pressure / physiology
Lactic Acid / blood
Male
Metabolic Networks and Pathways / physiology
Middle Aged
Monitoring, Physiologic
Oxygen Consumption / physiology
Subarachnoid Hemorrhage / complications*
Survival Rate
Vasospasm, Intracranial / complications,  physiopathology
Chemical
Reg. No./Substance:
50-21-5/Lactic Acid; 50-99-7/Glucose

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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