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Cited by 272

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Potassium-Induced Cortical Spreading Depressions during Focal Cerebral Ischemia in Rats: Contribution to Lesion Growth Assessed by Diffusion-Weighted NMR and Biochemical Imaging

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Busch, Elmar, Gyngell, Michael L., Eis, Manfred, Hoehn-Berlage, Mathias, Hossmann, Konstantin-Alexander·1996·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1097/00004647-199611000-00002
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Abstract

In focal ischemia of rats, the volume of ischemic lesion correlates with the number of peri-infarct depolarizations. To test the hypothesis that depolarizations accelerate infarct growth, we combined focal ischemia with externally evoked spreading depression (SD) waves. Ischemic brain infarcts were produced in halothane-anaesthetized rats by intraluminal thread occlusion of the middle cerebral artery (MCA). In one group of animals, repeated SDs were evoked at 15-min intervals by microinjections of potassium acetate into the frontal cortex. In another group, the spread of the potassium-evoked depolarizations was prevented by application of the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801). The volume of ischemic lesion was monitored for 2 h by diffusion-weighted imaging (DWI) and correlated with electrophysiological recordings and biochemical imaging techniques. In untreated rats, each microinjection produced an SD wave and a stepwise rise of the volume and signal intensity of the DWI-visible cortical lesion. The volume of this lesion increased between 15 min and 2 h of MCA occlusion from 19 ± 15% to 66 ± 16% of ipsilateral cortex. In dizocilpine-treated animals, microinjections of potassium did not evoke SDs, nor did the volume and signal intensity of the DWI-visible cortical lesion change. At 15 min after MCA occlusion, the DWI-visible lesion was larger than in untreated animals—43 ± 16% of the ipsilateral cortex; however, after 2 h, it increased only slightly further to 49 ± 21%. Slower lesion growth in the absence of SDs was also reflected by the volume of ATP-depleted tissue, which, after 2 h of MCA occlusion, involved 26 ± 12% of the ipsilateral cortex in treated and 49 ± 9% in untreated animals ( p < 0.01). These observations support the hypothesis that peri-infarct depolarizations accelerate cerebral infarct growth.

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Metadata

Authors
Busch, E., Gyngell, M. L., Eis, M., Hoehn-Berlage, M., & Hossmann, K.-A.
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
1996-11
Volume
16
Issue
6
Pages
1090-1099
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1097/00004647-199611000-00002
OpenAlex
W2088023851
Cited by
272
References
0
FWCI
9.25
Type
journal article
Language
en
Open access
bronze

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