Effects of graded reduction of brain blood flow on chemical control of breathing

Publisher Website
Google Scholar
Abstract
Ventilatory responses to CO2 and transient hypoxia were measured 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 (.DELTA..ovrhdot.VI/.DELTA.PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial O2 saturation (.DELTA..ovrhdot.VI/.DELTA.SaO2) was assessed by the transient N2 inhalation method. .DELTA..ovrhdot.VI/.DELTA.SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. .DELTA..ovrhdot.VI/.DELTA.PCO2 increased (0.94 .+-. 0.18 to 1.29 .+-. 0.24 l .cntdot. min-1 .cntdot. 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, .DELTA..ovrhdot.VI/.DELTA.PCO2 was depressed (0.38 .+-. 0.13 l .cntdot. min-1 .cntdot. 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. Moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2. .DELTA..ovrhdot.VI/.DELTA.PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed. Severe brain ischemia (50% BBF) blunts .DELTA..ovrhdot.VI/.DELTA.SaO2 and .DELTA..ovrhdot.VI/.DELTA.PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.