Nitric Oxide Modulates Spreading Depolarization Threshold in the Human and Rodent Cortex
Author(s) -
Gabor C. Petzold,
Stephan Haack,
Oliver von Bohlen und Halbach,
Josef Priller,
ThomasNicolas Lehmann,
Uwe Heinemann,
Ulrich Dirnagl,
Jens P. Dreier
Publication year - 2008
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.107.500710
Subject(s) - cortical spreading depression , medicine , extracellular , in vivo , pathogenesis , nitric oxide synthase , subarachnoid hemorrhage , nitric oxide , depolarization , ischemia , anesthesia , neuroscience , biology , biochemistry , migraine , microbiology and biotechnology
Recent clinical data have suggested that prolonged cortical spreading depolarizations (CSDs) contribute to the pathogenesis of delayed ischemic neurologic deficits after subarachnoid hemorrhage. Elevated extracellular potassium concentrations and lowered nitric oxide (NO) levels have been detected in experimental and clinical subarachnoid hemorrhage. We investigated whether a similar extracellular composition renders the brain more susceptible to CSDs.
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