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 ˙VE (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO(2) levels (0, 3.5 and 5% CO(2)). The regression line of the linear relationship between ˙V(E) and PETCO(2) (end-tidal CO(2)) 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 PETCO(2) was not shifted by LBNP-induced changes in PETCO2. However, changes in ˙V(E) from rest to LBNP were more related to changes in MCA V(mean) than changes in PETCO(2). 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 CO(2) from the brain causing hyperpnoea following activation of the central chemoreflex.