The ventilatory responses of conscious dogs to isocapnic oxygen tests. a method of exploring the central component of respiratory drive and its dependence on O2 and CO2.
Conscious unrestrained dogs trained to breathe through a respiratory mask or, after chronic tracheostomy, through a cuffed endotracheal tube were studied in an altitude chamber operated in such a way that end-tidal PO2 was maintained at 100, 75 or 60 Torr. Each hypoxic experiment was completed within 1 h of the onset of hypoxia. At all levels of oxygenation, resting pulmonary ventilation (V), obtained from the tidal volume (VT) and ventilatory period (T), and alveolar gas tensions (PAO2, PACO2) were measured cycle-by-cycle before and during isocapnic O2-tests (IOT) at various steady levels of alveolar PCO2 ranging from 30 to 48 Torr. For this, PCO2 in the inspired gas before and during IOT was adjusted so that PACO2 remained unchanged in the course of the first few breaths which followed the switch to hyperoxia. In analysing the transient changes of V in the course IOT, it was considered that an apnoea occurred when there was no measurable deflection on the integrated pneumotachogram past a duration twice the control T from the beginning of the last recorded ventilatory cycle. (1) Control V vs. PACO2 relationships showed classic positive interaction between hypercapnia and hypoxia; (2) during IOT at PAO2 of 100, 75 or 60 Torr, an apnoea occurred, V invariably falling to zero, provided that PACO2 was below 38-35 Torr according to the level of oxygenation; (3) above that threshold PACO2 value, the residual minimum ventilation (Vres) observed during IOT was linearly related to PACO2; (4) Vres vs. PACO2 relationships showed negative interaction between hypercapnia and hypoxia. It is concluded that (a) through isocapnic O2-tests, both the peripheral and central components of the ventilatory drive can be quantitatively estimated; (b) in conscious dogs, the pulmonary ventilation appears to be entirely driven by afferent activity from the arterial chemoreceptors, even in eucapnic normoxia; (c) the lower minimum ventilation seen in the course of O2-tests from a hypoxic rather than a normoxic background is still observed at PACO2 above normal, thus cannot be due only to hypocapnia related to preceding hypoxic hyperventilation must be caused by a central respiratory inhibition directly or indirectly related to depressant effect of even moderate hypoxia.
D000818:Animals; D001273:Atmosphere Exposure Chambers; D002245:Carbon Dioxide / Q000502:physiology; D002628:Chemoreceptor Cells / Q000502:physiology*; D004285:Dogs; D005260:Female; D000860:Hypoxia / Q000503:physiopathology*; D008168:Lung / Q000294:innervation / Q000502:physiology; D008297:Male; D010100:Oxygen / Q000502:physiology; D012119:Respiration; D013990:Tidal Volume; D013997:Time Factors
D002245:Carbon Dioxide; D010100:Oxygen