We have studied how in situ arterial (Pa-CO2) and brain tissue P-CO2 (
Pb-CO2) responses to acetazolamide (AZ) are affected by respiratory pa
tterns. Sixteen cats were anesthetized with ketamine. Group 1 cats (n
= 7) breathed air spontaneously. Group 2 cats (n = 6) were paralyzed a
nd ventilated mechanically to maintain Pa-CO2 at 37 +/- 1 Torr before
AZ administration; the respiratory rate and depth did not change durin
g the course of measurements. Two CO2 sensors to measure in situ Pa-CO
2 and Pb-CO2 continuously were used. One was placed through a burr hol
e into the cerebral white matter 15 mm in depth, and another was inser
ted into the femoral artery. After intravenous administration of AZ (2
0 mg/ kg), Pa-CO2 decreased, after a significant transient rise, and t
hen returned gradually to the baseline in group 1, but it increased gr
adually and reached a new steady state in group 2. Ph(CO2) and two gro
ups Immediately after administration. We conclude that AZ resulted in
a large increase in both Pb-CO2 and the Pb-CO2-Pa-CO2 gradient and tha
t there are two distinct In situ Pa-CO2 responses to AZ in spontaneous
ly breathing vs. mechanically ventilated animals. The mechanisms for t
hese observations are discussed.