Hypocapnia induced vasoconstriction significantly inhibits the neurovascular coupling in humans

Previous studies proved that vasodilation, caused by hypercapnia or acetazolamide, does not inhibit the visually evoked flow velocity changes in the posterior cerebral arteries. Our aim was to determine whether vasoconstriction induced by hypocapnia affects the neurovascular coupling.

By using a visual cortex stimulation paradigm, visually evoked flow velocity changes were detected by transcranial Doppler sonography in both posterior cerebral arteries of fourteen young healthy adults. The control measurement was followed by the examination under hyperventilation. Visual-evoked-potentials were also recorded during the control and hyperventilation phases.

The breathing frequency increased from 16 ± 2 to 37 ± 3/min during hyperventilation, resulting in a decrease of the end-tidal CO(2) from 37 ± 3 to 25 ± 3 mm Hg and decrease of resting peak systolic flow velocity from 58 ± 11 to 48 ± 11 cm/s (p<0.01). To allow comparisons between volunteers, relative flow velocity was calculated in relation to baseline. Repeated measures analysis of variance revealed significant difference between the relative flow velocity time courses during hyper- and normoventilation (p<0.001). The maximum changes of visually evoked relative flow velocities were 26 ± 7% and 12 ± 5% during normoventilation and hyperventilation, respectively (p<0.01). Visual-evoked-potentials did not differ in the control and hyperventilation phases.

The significantly lower visually evoked flow velocity changes but preserved visual-evoked-potential during hyperventilation indicates that the hypocapnia induced vasoconstriction significantly inhibits the neuronal activity evoked flow response.