Key result
Experimental SAH worsens neurological scores by ~16 points and reduces cerebral blood flow vs sham in mice.
Why the study?
Early brain injury significantly contributes to poor neurological outcomes and death after subarachnoid hemorrhage, but the underlying mechanisms and their relationship to serial cerebral blood flow changes in the ultra-early stages remain unclear.
Does experimental subarachnoid hemorrhage induce serial cerebral blood flow reductions and neurological symptom worsening in male ddY mice?
Does experimental subarachnoid hemorrhage induce serial cerebral blood flow reductions and neurological symptom worsening in male ddY mice?
Microthrombus formation peaks at 12 hours after experimental subarachnoid hemorrhage in mice, correlating with reduced cerebral blood flow and worsened neurological symptoms, which suggests a potential therapeutic target for early brain injury.
Ultra-early CBF changes may relate to neurological symptoms in mouse SAH; leaves open human EBI mechanism validation.
INTRODUCTION: Early Brain Injury (EBI) significantly contributes to poor neurological outcomes and death following subarachnoid hemorrhage (SAH). The mechanisms underlying EBI post-SAH remain unclear. This study explores the relationship between serial cerebral blood flow (CBF) changes and neurological symptoms, as well as the mechanisms driving CBF changes in the ultra-early stages after experimental SAH in mice. METHODS: SAH was induced by endovascular perforation in male ddY mice. Mice were sacrificed at 6, 12, 24, and 48 h after behavioral tests using the modified neurological score and grid walking test, and CBF was measured via Laser Speckle Flow Imaging (LSFI). Neurofunctional evaluation, CBF analysis, and Western blotting were used to assess SAH-induced damage. RESULTS: Neurological symptoms were significantly worse at 12 h post-SAH compared to sham (9.5 ± 1.7 vs. 25.6 ± 0.63, respectively; p < 0.0001). CBF was significantly reduced at 12 h post- SAH compared to sham (35.34 ± 8.611 vs. 91.06 ± 12.45, respectively; p < 0.0001). Western blotting revealed significantly elevated thrombin and matrix metalloproteinase 9 levels 12 h post-SAH (p < 0.05). CONCLUSION: Our results suggest that microthrombus formation peaked at 12 h post-SAH, potentially causing EBI and worsening neurological symptoms. Microthrombus formation in the ultraearly stages may represent a novel therapeutic target for managing EBI.
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Egashira et al. (2024) studied Experimental subarachnoid hemorrhage (SAH) and Early Brain Injury (EBI). Experimental subarachnoid hemorrhage via endovascular perforation vs. Sham procedure was evaluated on Modified neurological score and cerebral blood flow (CBF) at 12 hours post-SAH (p=<0.0001). Experimental SAH significantly worsened neurological scores (9.5 vs 25.6; p<0.0001) and reduced cerebral blood flow (35.34 vs 91.06; p<0.0001) at 12 hours compared to sham in mice.
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