Our data, in anesthetized rats, thus, indicate that relative hypoperfusion associated with hypoxemia adds an adverse effect based on ECoG. Total power of the signal, which represents global electrical activity, is significantly reduced. This is not the case when CBF response to hypoxemia is preserved (in the same animals).
A slowing of the frequencies of the ECoG content is present in this case. A balanced change in the frequency composition of ECoG (i.e. HGH FRAG 176-191 in high frequencies and increase in low frequencies) occurs at moderate levels of hypoxemia and are in keeping with known intracellular changes in excitability in response to an O2 sensing mechanism.
The effect of the vascular response to hypoxemia on the global amount of cortical electrical activity suggests important clinical consequences in patients with impaired cerebral circulation (OSA patients) or during adaptation to high altitude.
Additional studies using O2 free radicals modifiers (scavengers or transgenic animals) in our paradigm would give further insight on the mechanisms and cerebral consequences of hypoxemia.
