Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 41, Issue 2, Pages 413-430Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X20915801
Keywords
Blood-brain barrier; ketamine; seizure; spreading depolarization; stroke
Categories
Funding
- Deutsche Forschungsgemeinschaft [DFG HE 1128/18, DFG DR 323/5-1, DFG DR 323/10-1]
- NeuroCure EXC 257/2 Flexfund
- FP7 [602150 CENTER-TBI]
- Era-Net Neuron EBio2
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The study found that ketamine may help counteract the early progression of ischemic injury, reducing the onset of SDs, lesion volume, and neuronal injury.
Spreading depolarization (SD) and seizures are pathophysiological events associated with cerebral ischemia. Here, we investigated their role for injury progression in the cerebral cortex. Cerebral ischemia was induced in anesthetized male Wistar rats using the photothrombosis (PT) stroke model. SD and spontaneous neuronal activity were recorded in the presence of either urethane or ketamine/xylazine anesthesia. Blood-brain barrier (BBB) permeability, cerebral perfusion, and cellular damage were assessed through a cranial window and repeated intravenous injection of fluorescein sodium salt and propidium iodide until 4 h after PT. Neuronal injury and early lesion volume were quantified by stereological cell counting and manual and automated assessment of ex vivo T2-weighted magnetic resonance imaging. Onset SDs originated at the thrombotic core and invaded neighboring cortex, whereas delayed SDs often showed opposite propagation patterns. Seizure induction by 4-aminopyridine caused no increase in lesion volume or neuronal injury in urethane-anesthetized animals. Ketamine/xylazine anesthesia was associated with a lower number of onset SDs, reduced lesion volume, and neuronal injury despite a longer duration of seizures. BBB permeability increase inversely correlated with the number of SDs at 3 and 4 h after PT. Our results provide further evidence that ketamine may counteract the early progression of ischemic injury.
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