In situ arterial and brain tissue PCO2 responses to acetazolamide in cats

Abstract

We have studied how in situ arterial (PaCO2) and brain tissue PCO2 (PbCO2) responses to acetazolamide (AZ) are affected by respiratory patterns. Sixteen cats were anesthetized with ketamine. Group 1 cats (n = 7) breathed air spontaneously. Group 2 cats (n = 6) were paralyzed and ventilated mechanically to maintain PaCO2 at 37 +/- 1 Torr before AZ administration; the respiratory rate and depth did not change during the course of measurements. Two CO2 sensors to measure in situ PaCO2 and PbCO2 continuously were used. One was placed through a burr hole into the cerebral white matter 15 mm in depth, and another was inserted into the femoral artery. After intravenous administration of AZ (20 mg/kg), PaCO2 decreased, after a significant transient rise, and then returned gradually to the baseline in group 1, but it increased gradually and reached a new steady state in group 2. PbCO2 and the PbCO2-PaCO2 gradient increased remarkably in the two groups immediately after administration. We conclude that AZ resulted in a large increase in both PbCO2 and the PbCO2-PaCO2 gradient and that there are two distinct in situ PaCO2 responses to AZ in spontaneously breathing vs. mechanically ventilated animals. The mechanisms for these observations are discussed.