Basis of ionic dysregulation in cerebral ischemia

Arumugam, Thiruma V., Okun, Eitan and Mattson, Mark P. (2010). Basis of ionic dysregulation in cerebral ischemia. In Lucio Ammunziato (Ed.), New strategies in stroke intervention: Ionic transporters, pumps, and new channels (pp. 1-11) New York, United States: Humana Press. doi:10.1007/978-1-60761-280-3_1

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Author Arumugam, Thiruma V.
Okun, Eitan
Mattson, Mark P.
Title of chapter Basis of ionic dysregulation in cerebral ischemia
Title of book New strategies in stroke intervention: Ionic transporters, pumps, and new channels
Place of Publication New York, United States
Publisher Humana Press
Publication Year 2010
Sub-type Research book chapter (original research)
DOI 10.1007/978-1-60761-280-3_1
Series Contemporary Neuroscience
ISBN 978-1-60761-279-7
Editor Lucio Ammunziato
Chapter number 1
Start page 1
End page 11
Total pages 11
Total chapters 13
Collection year 2011
Language eng
Abstract/Summary Stroke causes 9% of all deaths around the world and is the second most common cause of death after ischemic heart disease. Enhancing recovery from stroke and limiting ischemic damage are major goals to decrease stroke morbidity and mortality . Brain tissue is extremely sensitive to oxygen and glucose deprivation, and even brief ischemia can initiate a complex sequence of events that ultimately culminates in cellular death. Studies performed during the past 30 years have identified several key pathophysiological events that lead to ischemic neuronal degeneration. The pathophysiological processes in stroke are complex and involve disruption of the blood–brain barrier (BBB), energy failure, loss of cell ion homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, free radical-mediated toxicity, generation of arachidonic acid products, cytokine-mediated apoptosis, activation of glial cells, and infiltration of leukocytes . In focal cerebral ischemia, ischemic tissue is divided into an infarction core and penumbra. The core is the area of the brain where blood flow is reduced below 10–20% of its normal levels . In the core, rapid anoxic depolarization causes immediate loss of membrane potential followed by the loss of membrane integrity and rapid necrotic cell death. The penumbra is the tissue surrounding the core where the blood flow is partly preserved due to collateral circulation and diffusion .
Keyword Stroke
Morbidity
Ischemic disease
Q-Index Code B1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Book Chapter
Collections: Official 2011 Collection
School of Biomedical Sciences Publications
 
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