Research ReportCerebral hemodynamic response to acute hyperoxia in awake mice

- Cerebral hemodynamic response to acute hyperoxia was investigated in awake mice.
- We measured the baseline CBF and hemodynamic response to whisker stimulation.
- We measured the cortical microvasculature by two-photon laser scanning microscopy.
- Hyperoxia caused vasoconstriction in arteriole and capillary, and decrease in CBF.
- Hyperoxia caused a rise of the increase in CBF evoked by sensory stimulation.

Cerebral hemodynamic response to acute hyperoxia was investigated in awake mice. Using laser-Doppler flowmetry (LDF), baseline cerebral blood flow (CBF) and the cerebrovascular responses to whisker stimulation were measured in awake mice during normoxia and hyperoxia. Using two-photon laser scanning microscopy (TPLSM), the changes in cortical microvasculature were measured during normoxia and hyperoxia. During hyperoxia (PaO2=482.3±19.7 mmHg), baseline CBF was 6.8% lower than normoxia (PaO2=97.3±6.0 mmHg). The degree of increase in CBF evoked by whisker stimulation was greater during hyperoxia (18.1±5.0%) than normoxia (13.1±3.5%) (P<0.05). TPLSM imaging of the somatosensory cortex showed vasconstriction in arterioles and capillaries during hyperoxia. Since the effective diffusivity for oxygen in the capillary bed might decrease by hyperoxia due to a decrease in capillary blood volume according to Hyder׳s model, an increase in the cerebral metabolic rate of oxygen utilization by neural activation during hyperoxia might need a greater increase in CBF as compared with normoxia. The hemodynamic response to neural activation could be modified by acute hyperoxia due to modification of the relation between changes in CBF and oxygen consumption by neural activation.