Correlation of the extracellular glutamate concentration with extent of blood flow reduction after subdural hematoma in the rat

Bullock, Ross; Butcher, Steve P.; Chen, Min-Hsiung; Kendall, Lee G.; McCulloch, James

doi:10.3171/jns.1991.74.5.0794

Cited by 145 publications

(50 citation statements)

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“…Studies conducted by Katayama, et al, [28] Faden, et al, [17] and our own previous studies have shown brief, transient elevations of EAAs to two to seven times higher than basal levels, persisting only 10 to 30 minutes after impact, in both fluid percussion injury and subdural hematoma in the rat. [6,8,12] Animal studies have only assessed events over a few hours before and after impact. In contrast, these human studies have only captured data for the postimpact period, ranging from 3 hours to 6 days after impact.…”

Section: Structural Amino Acids Eaas and Causes Of Releasementioning

confidence: 99%

“…[3,6,10,11,17,22,49] Following the comparatively recent discovery of this role, it has become a focus of major neuroscientific interest because of its potential role in the causation of both acute and chronic neuronal damage. In 1983, Rothman and Olney[46] proposed the "excitotoxic" hypothesis.…”

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confidence: 99%

“…[3,6,11,22,23,43,49] In these models, a variety of drugs that block the effects of glutamate both presynaptically and at postsynaptic receptor sites have reduced both ischemic brain damage and glutamate release. [5,7,12,20,21,24,25,29,32,33,36,40,53,55,56] There are now several Phase II and Phase III trials in progress to evaluate the efficacy of glutamate antagonist drugs in both neurotrauma and stroke.…”

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confidence: 99%

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Factors affecting excitatory amino acid release following severe human head injury

Bullock¹,

Zauner²,

Woodward³

et al. 1998

FOC

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Recent animal studies demonstrate that excitatory amino acids (EAAs) play a major role in neuronal damage after brain trauma and ischemia. However, the role of EAAs in patients who have suffered severe head injury is not understood. Excess quantities of glutamate in the extracellular space may lead to uncontrolled shifts of sodium, potassium, and calcium, disrupting ionic homeostasis, which may lead to severe cell swelling and cell death. The authors evaluated the role of EEAs in human traumatic brain injury. In 80 consecutive severely head injured patients, a microdialysis probe was placed into the gray matter along with a ventriculostomy catheter or an intracranial pressure (ICP) monitor for 4 days. Levels of EAAs and structural amino acids were analyzed using high-performance liquid chromatography. Multifactorial analysis of the amino acid pattern was performed and its correlations with clinical parameters and outcome were tested. The levels of EAAs were increased up to 50 times normal in 30% of the patients and were significantly correlated to levels of structural amino acids both in each patient and across the whole group (p < 0.01). Secondary ischemic brain injury and focal contusions were most strongly associated with high EAA levels (27 ± 22 μmol/L). Sustained high ICP and poor outcome were significantly correlated to high levels of EAAs (glutamate > 20 μmol/L; p < 0.01). The release of EAAs is closely linked to the release of structural amino acids and may thus reflect nonspecific development of membrane micropores, rather than presynaptic neuronal vesicular exocytosis. The magnitude of EAA release in patients with focal contusions and ischemic events may be sufficient to exacerbate neuronal damage, and these patients may be the best candidates for treatment with glutamate antagonists in the future.

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Section: Structural Amino Acids Eaas and Causes Of Releasementioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Factors affecting excitatory amino acid release following severe human head injury

Bullock¹,

Zauner²,

Woodward³

et al. 1998

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“…Several animal studies applying microdialysis in neuronal injury models have been conducted. [2][3][4] More recently, microdialysis found its way into neurological intensive care units as a tool for monitoring metabolism and neuronal injury in subarachnoid hemorrhage 5 and severe head injury. 6 Only very limited data are present on microdialysis in ischemic stroke.…”

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Neurochemical Monitoring of Fatal Middle Cerebral Artery Infarction

Berger

Annecke

Aschoff

et al. 1999

Stroke

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Background-Microdialysis is a method for neurochemical monitoring that has been applied more frequently over the past few years in patients suffering from subarachnoid hemorrhage, acute brain injury, and stroke. It is used to study the course of extracellular molecules of low molecular weight, such as excitatory amino acids or metabolic end products. Case Description-We report the case of a 43-year-old patient suffering from left hemispheric stroke with a space-occupying postischemic edema leading to a considerable mass effect on the contralateral side. For treatment of severe edema, hypothermia was initiated. The microdialysis and intracranial pressure probe were placed into the noninfarcted hemisphere. A massive increase in levels of glutamate, glycerine, and the lactate-pyruvate ratio was measured 24 hours before intracranial pressure elevation was observed and brain death occurred. Conclusions-Monitoring excitatory amino acids, glycerine as a membrane component, and lactate-pyruvate ratio as an energy marker by microdialysis is a useful tool to increase our understanding of biochemical events in secondary brain damage. For future prevention of secondary ischemia in patients with massive stroke, close neurochemical monitoring might be valuable to improve therapy, particularly in the critically ill. (Stroke. 1999;30:460-463.)Key Words: cerebral infarction Ⅲ cerebral ischemia Ⅲ glutamates Ⅲ microdialysis Ⅲ middle cerebral artery B rain ischemia is associated with an excessive release of excitatory amino acids, such as glutamate or aspartate, and with a shift of energy-related metabolites from the intracellular to the extracellular fluid. Intracerebral microdialysis 1 is a method by which these endogenous substances can be extracted from the extracellular fluid into a dialysate in which relative changes in concentration of these substances can be measured. Several animal studies applying microdialysis in neuronal injury models have been conducted. [2][3][4] More recently, microdialysis found its way into neurological intensive care units as a tool for monitoring metabolism and neuronal injury in subarachnoid hemorrhage 5 and severe head injury. 6 Only very limited data are present on microdialysis in ischemic stroke.In this case report, we demonstrate a massive increase in extracellular glutamate, glycerine, and the lactate-pyruvate ratio as a consequence of secondary brain damage in a patient with a fatal middle cerebral artery (MCA) infarction. Subjects and MethodsThis study was approved by the local Ethics Committee (approval number 34/97).A 10-mm flexible microdialysis probe with an external diameter of 0.5 mm (CMA/70 custom probe, CMA/Microdialysis), and an intracranial pressure (ICP) measuring device (Spiegelberg AG) were inserted into the parietal parenchyma of the healthy hemisphere. A thermistor attached to the ICP device allowed continuous recording of brain temperature. 7 A second microdialysis probe (CMA/60) placed into the abdominal subcutaneous tissue served as a reference.In the neurological criti...

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“…The progression to infarction despite adequate CPP may be explained by altered autoregulation, direct toxicity from blood, or neurochemical alterations. For example, experimental models of traumatic hematoma [6] or diffuse axonal injury [13] and clinical studies [1] demonstrate that levels of excitatory amino acids, such as glutamate, which in high concentrations appear integral to the pathophysiological mechanism of neuron injury and death in cerebral ischemia, [27] are increased after head injury and may alter membrane permeability through activation of ligand-gated channels. Similarly, following injury, direct mechanical stimulation can cause ionic fluxes and neuron firing.…”

Section: Cerebral Perfusion Pressure and Cerebral Infarctionmentioning

confidence: 99%

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Correlation of the extracellular glutamate concentration with extent of blood flow reduction after subdural hematoma in the rat

Cited by 145 publications

References 24 publications

Factors affecting excitatory amino acid release following severe human head injury

Factors affecting excitatory amino acid release following severe human head injury

Neurochemical Monitoring of Fatal Middle Cerebral Artery Infarction

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