Ventilatory response in metabolic acidosis and cerebral blood volume in humans.
SourceRespiration Physiology, 124, 2, (2001), pp. 105--15
Article / Letter to editor
Display more detailsDisplay less details
SubjectBloodpressure regulation, tissue oxygenation and exercise; Control mechanisms in asthma and chronic obstructive pulmonary disease.; Bloeddrukregulatie, weefseloxygenatie en inspanning; Overig onderzoek geriatrie; Regulatie mechanismen bij astma en chronisch obstructieve longaandoeningen
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 (5610 years) were investigated. To induce metabolic acidosis, ammonium chloride (NH(4)Cl) was given orally. CBV was measured using Near Infrared Spectroscopy during normo- and hypercapnia and related to inspired ventilation (V(i)). A mean acute metabolic acidosis of Delta pH - 0.04 was realized with a mean decreased arterialized capillary PCO(2) (P(c)CO(2)) of 0.20 kPa (1.5 mmHg) (both P<0.001). During normocapnia, CBV was 3.510.71 and 3.650.56 ml 100 g(-1) (meanS.D.), measured under neutral metabolic conditions and during acute metabolic acidosis, respectively (ns). Corresponding values of V(i) were 7.61.4 and 10.02.4 l min(-1) (P<0.01), respectively. The slopes of the CO(2)-responsiveness (DeltaCBV/DeltaP(c)CO(2) and DeltaV(i)/DeltaP(c)CO(2)), were not significantly different during both metabolic conditions. A significant correlation between DeltaCBV/DeltaP(c)CO(2) and DeltaV(i)/DeltaP(c)CO(2) 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.
Upload full text