Ventilatory response in metabolic acidosis and cerebral blood volume in humans

The relationship between alterations in cerebral blood volume (CBV) and central chemosensitivity regulation was studied under neutral metabolic conditions and during metabolic acidosis. Fifteen healthy subjects (56±10 years) were investigated. To induce metabolic acidosis, ammonium chloride (NH4Cl) was given orally. CBV was measured using Near Infrared Spectroscopy during normo- and hypercapnia and related to inspired ventilation (V̇i). A mean acute metabolic acidosis of ΔpH −0.04 was realized with a mean decreased arterialized capillary Pco2 (Pcco2) of 0.20 kPa (1.5 mmHg) (both P<0.001). During normocapnia, CBV was 3.51±0.71 and 3.65±0.56 ml 100 g−1 (mean±S.D.), measured under neutral metabolic conditions and during acute metabolic acidosis, respectively (ns). Corresponding values of V̇i were 7.6±1.4 and 10.0±2.4 l min−1 (P<0.01), respectively. The slopes of the CO2-responsiveness (ΔCBV/ΔPcco2 and ΔV̇i/ΔPcco2), were not significantly different during both metabolic conditions. A significant correlation between ΔCBV/ΔPcco2 and ΔV̇i/ΔPcco2 was found during metabolic acidosis (P<0.01), but not under neutral metabolic conditions. CBV does not contribute in a predictable way to the regulation of central chemoreceptors.