EFFECTS OF GRADED REDUCTION OF BRAIN BLOOD-FLOW ON CHEMICAL CONTROL OF BREATHING

We measured ventilatory responses to CO2 (ΔVI/ΔPCO2) and transient hypoxia (ΔVI/ΔSaO2) during reductions of brain blood flow (BBF) to 70 and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (ΔVI/ΔPCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (ΔVI/SaO2) was assessed by the transient N2 inhalation method. ΔVI/ΔSaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. ΔVI/ΔPCO2 increased (0.94 ± 0.18 to 1.29 ± 0.24 l/min-1/Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. AT 50% BBF, ΔVI/ΔPCO2 was depressed (0.38 ± 0.13 l/min-1/Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) ΔVI/ΔPCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts ΔVI/ΔSaO2 and ΔVI/ΔPCO2, probably as a consequence of hypoxic depression of the respiratory neurons.