Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA V_mean (middle cerebral artery mean blood velocity) and V̇_E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO₂ levels (0, 3.5 and 5% CO₂). The regression line of the linear relationship between V̇_E and PETCO₂ (end-tidal CO₂) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA V_mean and PETCO₂ was not shifted by LBNP-induced changes in PETCO₂. However, changes in V̇_E from rest to LBNP were more related to changes in MCA V_mean than changes in PETCO₂. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO₂ from the brain causing hyperpnoea following activation of the central chemoreflex.