Document Detail


Electrochemical Failure of the Brain Cortex Is More Deleterious When it Is Accompanied by Low Perfusion.
MedLine Citation:
PMID:  23287786     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: Clinical and experimental evidence suggests that spreading depolarization facilitates neuronal injury when its duration exceeds a certain time point, termed commitment point. We here investigated whether this commitment point is shifted to an earlier period, when spreading depolarization is accompanied by a perfusion deficit. METHODS: Electrophysiological and cerebral blood flow changes were studied in a rat cranial window model followed by histological and immunohistochemical analyses of cortical damage. RESULTS: In group 1, brain topical application of artificial cerebrospinal fluid (ACSF) with high K(+) concentration ([K(+)](ACSF)) for 1 hour allowed us to induce a depolarizing event of fixed duration with cerebral blood flow fluctuations around the baseline (short-lasting initial hypoperfusions followed by hyperemia). In group 2, coapplication of the NO-scavenger hemoglobin ([Hb](ACSF)) with high [K(+)](ACSF) caused a depolarizing event of similar duration, to which a severe perfusion deficit was coupled (=spreading ischemia). In group 3, intravenous coadministration of the L-type calcium channel antagonist nimodipine with brain topical application of high [K(+)](ACSF)/[Hb](ACSF) caused spreading ischemia to revert to spreading hyperemia. Whereas scattered neuronal injury occurred in the superficial cortical layers in the window areas of groups 1 and 3, necrosis of all layers with partial loss of the tissue texture and microglial activation were observed in group 2. CONCLUSIONS: The results suggest that electrochemical failure of the cortex is more deleterious when it is accompanied by low perfusion. Thus, the commitment point of the cortex is not a universal value but depends on additional factors, such as the level of perfusion.
Authors:
Jens P Dreier; Ilya V Victorov; Gabor C Petzold; Sebastian Major; Olaf Windmüller; Francisco Fernández-Klett; Mahesh Kandasamy; Ulrich Dirnagl; Josef Priller
Related Documents :
24708926 - Cntf regulates neurite outgrowth and neuronal migration through jak2/stat3 and pi3k/akt...
23859966 - Therapeutic drug approach to stimulate clinical recovery after brain injury.
24173566 - Glial cells phagocytose neuronal debris during the metamorphosis of the central nervous...
23755116 - The expression of ghs-r in primary neurons is dependent upon maturation stage and regio...
7884466 - Functional organization of sound direction and sound pressure level in primary auditory...
19566496 - Visual evoked potential and spatial frequency in migraine: a longitudinal study.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-1-3
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  -     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-1-4     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
From the Center for Stroke Research Berlin.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Smoking-thrombolysis paradox: recanalization and reperfusion rates after intravenous tissue plasmino...
Next Document:  Elevated homocysteine and carotid plaque area and densitometry in the Northern Manhattan Study.