Please use this identifier to cite or link to this item:
Title: Malignant edema formation following transient MCA occlusion : decrease of cerebral perfusion pressure causes secondary elevation of glutamate
Authors: Toyota, Shingo
Graf, Rudolf
Valentino, Mario
Dohmen, Christian
Wienhard, K.
Heiss, Wolf-Dieter
Keywords: Edema, Malignant
Cerebral edema
Issue Date: 2001
Publisher: Raven Press Publishers
Citation: Toyota, S., Graf, R., Valentino, M., Dohmen, C., Wienhard, K., & Heiss, W. D. (2001). Malignant edema formation following transient MCA occlusion: decrease of cerebral perfusion pressure causes secondary elevation of glutamate. Journal of Cerebral Blood Flow and Metabolism, 21, S157-S157.
Abstract: Malignant, space-occupying brain edema is a relevant, serious complication in various clinical situations including large hemispheric stroke. In the search for intensive monitoring tools that permit early identification of such fatal outcome, microdialysis has recently been introduced in patient care. Furthermore, to date, the role of neuroactive substances in malignant edema remains obscure. We therefore examined the correlation between secondary perfusional disturbance assessed by monitoring cerebral perfusion pressure (CPP) and secondary elevation of glutamate and other neuroactive substrates in a reperfusion injury model in cats that was produced by 3 hours middle cerebral artery occlusion followed by 6 hours reperfusion.
Appears in Collections:Scholarly Works - FacM&SPB

Items in OAR@UM are protected by copyright, with all rights reserved, unless otherwise indicated.