Ventral medullary pH and ventilatory responses to hyperperfusion and hypoxia

The role of a sudden increase in brain perfusion on ventral medullary surface pH (Vm pH) and minute ventilation (V̇I) was assessed in anesthetized peripherally chemodenervated cats. Acute hypertension (AH), produced by rapid inflation of an aortic balloon, and hypoxemia, produced with either inhalation of 1% CO (COHx) or inhalation of a hypoxic gas (HHx), were used to increase brain blood flow. In the AH group, increasing arterial blood pressure (from 122 ± 3 to 180 ± 5 mmHg) caused a rapid (<5 s) increase in Vm pH in every trial (n = 18). Associated with the mean peak increases in Vm pH (0.003 ± 0.0004 pH units) were significant decreases in tidal volume (7-9%). In the COHx group, 17% HbCO caused a significant increase in Vm pH (0.003 ± 0.0005 pH unit) and diminution of V̇I (9%). Further increases in HbCO caused a progressive ventral medullary acidosis and greater reductions in V̇I. The results from the HHX group were qualitatively similar to the COHx group; there was a biphasic response of Vm pH, i.e., an initial increase in Vm pH (0.008 ± 0.001) followed by a steady decrease in Vm pH, with reductions in V̇I associated with both phases. We conclude that 1) hyperperfusion, per se, produces an increase in Vm pH and a reduction in V̇I equivalent in magnitude to that predicted from the CO₂ stimulus-response curve; 2) the alkalotic shift in Vm pH and concomitant diminution in V̇I associated with mild hypoxia is probably related to an increase in ventral medullary perfusion; and 3) the ventilatory depression associated with the medullary acidosis of moderate brain hypoxia must be attributed to another mechanism.