These two elements can play roles either together or separately in secondary impairments such as brain oedema, increase in intracranial pressure, neurocyte injury and decreased perfusion in the local brain and affected hemisphere.
On the other hand, oxidative stress response can cause neurocyte damage and endothelial apoptosis, which can reduce eNOS and nNOS in the corpus cavernosum, and these can decrease NO and then lead to DMED [51, 52].
An idea, according to which the lack of glucose may have more importance for neurocyte functioning than ketone activity, has also been taken into consideration [31].
This also resulted in more intercellular space among the neurocytes. Moreover, the neurocyte cells under the experiments of high-dose rare-earth nanoparticles were decreased compared to control group, as shown in [Figure 4].