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Gross observation of the whole brains following bTBI induced by moderate blast showed brain edema without focal lesions, contusion, or subarachnoid hemorrhage [Figure 5]b.
[Figure 6] displays the neurological outcomes after bTBI induced by moderate blast.
No significant difference was found in the amount of EB dye among sham bTBI [Figure 2]a; 44.9 [+ or -] 0.8 [micro]g/wet brain], bTBI 1 day (44.9 [+ or -] 0.4 [micro]g/wet brain, t = −0.06, P > 0.05), bTBI 2 days (44.6 [+ or -] 0.3 [micro]g/wet brain, t = −0.68, P > 0.05), and bTBI 3-day groups (47.5 [+ or -] 1.3 [micro]g/wet brain, t = 2.89, P > 0.05), indicating little discrepancy of the BBB.
As shown in [Figure 2]d, after bTBI was induced by moderate explosion, the degree of brain edema increased significantly at 1 day (76.9% [+ or -] 1.3% vs.
2 [+ or -] 1/HPF, t = 6.1, P < 0.001) after bTBI in the frontal lobe [Figure 7].
The apoptosis indexes of bTBI 1 day (25.06% [+ or -] 2.15% vs.
Interface astroglial scarring at boundaries between brain parenchyma and fluids, and at junctions between gray and white matter, has been detected exclusively in blast-exposed brain specimens. Here, the expression of GFAP determined the astrocyte activation after bTBI. Interestingly, GFAP positive expression was detected around the ventricles of the brain, around the blood vessels, and in the brainstem and hippocampus compared with sham bTBI group [Figure 10].
Development of subarachnoid hemorrhage, brain edema, hyperemia, and delayed vasospasm are very common for the patients suffering from moderate to severe bTBI. Analogously, subarachnoid hemorrhage and brain edema were detected both by CT scan and gross observation.
Spatial memory and motor activity abnormalities were observed obviously at 1 day post-bTBI, perhaps reflecting the pathophysiology of bTBI. This speculation requires further research.
In general, neuronal, axonal, and glial injuries have all been observed following single-blast exposure.,,, H and E staining indicated the most necrotic cells in the frontal lobe and hippocampus at 3 days after bTBI induced by moderate intensity shock wave.
Our results show that the decrease in brain compliance by increase in ICP can alleviate brain damage not only in the blunt trauma induced TBI but also in bTBI, in this case likely by mitigating the contribution of skull flexure to the interaction of brain with the cranium.
In conclusion, the present study indicates that IJV compression has a protective potential in bTBI by attenuating blast-induced neurodegeneration, edema, oxidative damage, and vascular dysfunction.
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