Electroencephalogram (EEG) Alpha Power as a Marker of Visuospatial Attention Orienting and Suppression in Normoxia and Hypoxia. An Exploratory Study

While electroencephalogram (EEG) alpha desynchronization has been related to anticipatory orienting of visuospatial attention, an increase in alpha power has been associated to its inhibition. A separate line of findings indicated that alpha is affected by a deficient oxygenation of the brain or hypoxia, although leaving unclear whether the latter increases or decreases alpha synchronization. Here, we carried out an exploratory study on these issues by monitoring attention alerting, orienting, and control networks functionality by means of EEG recorded both in normoxia and hypoxia in college students engaged in four attentional cue-target conditions induced by a redesigned Attention Network Test. Alpha power was computed through Fast Fourier Transform. Regardless of brain oxygenation condition, alpha desynchronization was the highest during exogenous, uncued orienting of spatial attention, the lowest during alerting but spatially unpredictable, cued exogenous orienting of attention, and of intermediate level during validly cued endogenous orienting of attention, no matter the motor response workload demanded by the latter, especially over the left hemisphere. Hypoxia induced an increase in alpha power over the right-sided occipital and parietal scalp areas independent of attention cueing and conflict conditions. All in all, these findings prove that attention orienting is undergirded by alpha desynchronization and that alpha right-sided synchronization in hypoxia might sub-serve either the effort to sustain attention over time or an overall suppression of attention networks functionality.

In vitro and in vivo kinetic handling of nitrite in blood: effects of varying hemoglobin oxygen saturation

Growing evidence suggests that nitrite, acting via reduction to nitric oxide by deoxyhemoglobin, may play an important role in local control of blood flow during hypoxia. To investigate the effect of hypoxia (65 Torr arterial Po2) on the kinetic properties of nitrite, a bolus injection of sodium nitrite (10 mg/kg iv) was given to normoxic or hypoxic newborn lambs, and the time course of plasma nitrite and methemoglobin (MetHb) concentrations was measured. The in vivo kinetics of nitrite disappearance from plasma were biphasic and were not affected by hypoxia. Changes in MetHb, a product of the nitrite-hemoglobin reaction, also did not differ with the level of oxygenation. Hypoxia potentiated the hypotensive effects of nitrite on pulmonary and systemic arterial pressures. The disappearance of nitrite from plasma was equivalent to the increase in MetHb on a molar basis. In contrast, nitrite metabolism in sheep blood in vitro resulted in more than one MetHb per nitrite equivalent under mid- and high-oxygenation conditions: oxyhemoglobin (HbO2) saturation = 50.3 ± 1.7% and 97.0 ± 1.3%, respectively. Under the low-oxygenation condition (HbO2 saturation = 5.2 ± 0.9%), significantly less than 1 mol of MetHb was produced per nitrite equivalent, indicating that a significant portion of nitrite is metabolized through pathways that do not produce MetHb. These data support the idea that the vasodilating effects of nitrite are potentiated under hypoxic conditions due to the reduction of nitrite to nitric oxide by deoxyhemoglobin.