학술논문
Cerebrospinal fluid is a significant fluid source for anoxic cerebral oedema.
Document Type
Journal Article
Author
Du, Ting; Mestre, Humberto; Kress, Benjamin T; Liu, Guojun; Sweeney, Amanda M; Samson, Andrew J; Rasmussen, Martin Kaag; Mortensen, Kristian Nygaard; Bork, Peter A R; Peng, Weiguo; Olveda, Genaro E; Bashford, Logan; Toro, Edna R; Tithof, Jeffrey; Kelley, Douglas H; Thomas, John H; Hjorth, Poul G; Martens, Erik A; Mehta, Rupal I; Hirase, Hajime
Source
Subject
*CEREBRAL edema
*CEREBROSPINAL fluid
*THERAPEUTIC hypothermia
*EDEMA
*CARDIAC arrest
*INDUCED hypothermia
*BRAIN
*RESEARCH
*ANIMAL experimentation
*RESEARCH methodology
*EVALUATION research
*COMPARATIVE studies
*CEREBRAL anoxia
*MICE
*DISEASE complications
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Language
ISSN
0006-8950
Abstract
Cerebral oedema develops after anoxic brain injury. In two models of asphyxial and asystolic cardiac arrest without resuscitation, we found that oedema develops shortly after anoxia secondary to terminal depolarizations and the abnormal entry of CSF. Oedema severity correlated with the availability of CSF with the age-dependent increase in CSF volume worsening the severity of oedema. Oedema was identified primarily in brain regions bordering CSF compartments in mice and humans. The degree of ex vivo tissue swelling was predicted by an osmotic model suggesting that anoxic brain tissue possesses a high intrinsic osmotic potential. This osmotic process was temperature-dependent, proposing an additional mechanism for the beneficial effect of therapeutic hypothermia. These observations show that CSF is a primary source of oedema fluid in anoxic brain. This novel insight offers a mechanistic basis for the future development of alternative strategies to prevent cerebral oedema formation after cardiac arrest. [ABSTRACT FROM AUTHOR]