Abstract TP275: Brain Cell Volume Reductions After Severe Ischemic and Hemorrhagic Strokes in Rat

Autor: Frederick Colbourne, Ian R. Winship, Yonglie Ma, Cassandra M. Wilkinson, Anna C J Kalisvaart, Tiffany F. C. Kung
Rok vydání: 2020
Předmět:
Zdroj: Stroke. 51
ISSN: 1524-4628
0039-2499
DOI: 10.1161/str.51.suppl_1.tp275
Popis: Background: Raised intracranial pressure (ICP) following severe strokes can impede blood flow to the brain, causing injury or death. There are compensatory mechanisms regulating ICP, but they are often inadequate. Interestingly, our recent observations in intracerebral hemorrhage (ICH) suggest that a volume reduction in remaining brain may serve a compensatory role after large strokes. We observed neurons well outside the hematoma reduce their volume and intercellular space 7 days after the bleed. Here, we tested the hypotheses that this volume reduction would occur sooner in both ischemic and hemorrhagic insults. Methods: Rats received either an ICH via stereotaxic infusion of collagenase or a sham procedure. Euthanasia and perfusion fixation occurred either 1 (N=12), 3 (N=12), or 7 (N=12) days following the ICH. Following histological processing, cellular volume, density, and cortical thickness were assessed with stereological techniques in representative brain regions such as hippocampus, striatum, and primary somatosensory cortex (S1). In a separate experiment, rats received either a middle cerebral artery occlusion (MCAO) via intraluminal suture occlusion (N=8), or a sham procedure (N=7). Rats were euthanized and perfusion fixed 1 day following the MCAO, with brains processed and assessed as described above. Results: After ICH, the decrease in neuronal volume (up to 60%) compared to shams had the largest effect one day following the insult in hippocampal layers CA1 and CA3 (p Discussion: Our data challenges the assumption that ‘healthy’ brain tissue outside the injured area maintains its volume after stroke. Given the magnitude of cell volume reductions, we posit that this is an important intracranial compliance mechanism invoked after severe strokes.
Databáze: OpenAIRE