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DC Field | Value | Language |
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dc.contributor.author | Toyota, Shingo | - |
dc.contributor.author | Graf, Rudolf | - |
dc.contributor.author | Dohmen, Christian | - |
dc.contributor.author | Valentino, Mario | - |
dc.contributor.author | Grond, Martin | - |
dc.contributor.author | Wienhard, Klaus | - |
dc.contributor.author | Heiss, Wolf-Dieter | - |
dc.date.accessioned | 2018-02-08T14:10:31Z | - |
dc.date.available | 2018-02-08T14:10:31Z | - |
dc.date.issued | 2001 | - |
dc.identifier.citation | Toyota, S., Graf, R., Dohmen, C., Valentino, M., Grond, M., Wienhard, K., & Heiss, W. D. (2001). Elevation of extracellular glutamate in the final, ischemic stage of progressive epidural mass lesion in cats. Journal of Neurotrauma, 18(12), 1349-1357. | en_GB |
dc.identifier.uri | https://www.um.edu.mt/library/oar//handle/123456789/26607 | - |
dc.description.abstract | Epidural mass lesions may cause ischemia due to progressive intracranial hypertension. In order to investigate the impact of intracranial pressure on accumulation of neuroactive substances, we gradually raised intracranial pressure in five halothane anesthetized cats by inflation of an epidural balloon. We evaluated in the parietal cortex contralateral to the site of balloon inflation, alterations of extracellular glutamate and purine catabolites and of the lactate/pyruvate ratio in relation to changes of intracranial, cerebral perfusion and mean arterial blood pressure. In a complementary experiment, regional cerebral blood flow was assessed by sequential positron emission tomography. In this simplified mass lesion model, extracellular glutamate increased in all cats at a late, critical stage after tentorial herniation, when intracranial pressure had increased to more than 90 mm Hg, cerebral perfusion pressure had decreased below 40–50 mm Hg. Positron emission tomography assess- ments revealed that the ischemic threshold for glutamate accumulation was in the range of 15–20 mL/100 g/min. Purine catabolites and the lactate/pyruvate ratio increased somewhat earlier than glutamate, but also after reaching the critical, terminal stage. We conclude that in this model of progressive epidural compression, glutamate-mediated excitotoxic processes at sites remote from the initial focal lesion depend on processes such as delayed ischemia in combination with tentorial herniation and systemic hypotension. These processes seem to be initiated by a decrease of cerebral perfusion pressure below a threshold of 40–50 mm Hg. | en_GB |
dc.language.iso | en | en_GB |
dc.publisher | Mary Ann Liebert Inc. | en_GB |
dc.rights | info:eu-repo/semantics/restrictedAccess | en_GB |
dc.subject | Intracranial pressure | en_GB |
dc.subject | Brain microdialysis | en_GB |
dc.subject | Cerebral ischemia -- Diagnosis | en_GB |
dc.subject | Intracranial hypertension | en_GB |
dc.subject | Glutamic acid | en_GB |
dc.title | Elevation of extracellular glutamate in the final, ischemic stage of progressive epidural mass lesion in cats | en_GB |
dc.type | article | en_GB |
dc.rights.holder | The copyright of this work belongs to the author(s)/publisher. The rights of this work are as defined by the appropriate Copyright Legislation or as modified by any successive legislation. Users may access this work and can make use of the information contained in accordance with the Copyright Legislation provided that the author must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the prior permission of the copyright holder | en_GB |
dc.description.reviewed | peer-reviewed | en_GB |
dc.identifier.doi | 10.1089/08977150152725641 | - |
dc.publication.title | Journal of Neurotrauma | en_GB |
Appears in Collections: | Scholarly Works - FacM&SPB |
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Elevation_of_extracellular_glutamate_in_the_final_ischemic_stage_2001.pdf Restricted Access | 375.76 kB | Adobe PDF | View/Open Request a copy |
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