[Effects of cerebral blood flow on hypoxic ventilatory response--a human study by jugular venous blood sampling]

To assess the effect of cerebral blood flow on hypoxic ventilatory response in humans, internal jugular venous blood and arterial blood gases and ventilation were measured simultaneously and repeatedly in fifteen healthy male volunteers in two settings: 1) progressive and subsequent sustained isocapnic hypoxia (PetO2 = 45 Torr), and 2) stepwise and progressive hypercapnia. Jugular venous-arterial PCO2 difference decreased significantly from 8.7 Torr at control to 7.4 Torr at 1 min, and 6.4 Torr at 5 and 15 min of sustained hypoxia, probably due to the increase in cerebral blood flow. Corrected hypoxic ventilatory response (HVR) (1.27 +/- 0.75 1/min/%), which was calculated with the product of change in jugular venous PCO2 (PjCO2) and the value of hypercapnic ventilatory response on PjCO2 (delta VE/delta PjCO2), was significantly higher than the actually measured HVR (0.52 +/- 0.45 1/min/%). However, the magnitude of this correction did not correlate with the original HVR. Ventilation decreased significantly during sustained hypoxia from 16.5 +/- 5.3 1/min at 1 min to 14.1 +/- 6.9 1/min (p less than 0.05) at 15 min of hypoxia. Such ventilatory depression was remarkable in the low responders, whose HVR were lower than the average response of all subjects. However, the behavior of PaO2 and PjCO2 did not seem to explain those results. Therefore, we conclude that an increase in cerebral blood flow may have a significant effect on HVR in humans even during moderate isocapnic hypoxia (PaO2 = 45 Torr), but it is unlikely to be the main factor of the inter-individual variation in HVR nor the ventilatory depression during sustained hypoxia.