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.