Carbonic anhydrase activity of rabbit lungs

Pulmonary carbonic anhydrase (CA) activity was studied in rabbit lungs perfused with solutions containing no CA. Measurements were made of the amount of ¹⁴CO₂ appearing in the expired gas following injections of H¹⁴CO₃^-, ¹⁴CO₂, or a 20:1 mixture of each into the pulmonary artery. The fraction of the injected label in the expired gas was only 17% greater for ¹⁴CO₂ than for the mixture, suggesting that equilibration between H¹⁴CO₃^- and ¹⁴CO₂ was nearly complete during the capillary transit time. Inhibition of pulmonary CA decreased the excretion of H¹⁴CO₃^- and the mixture by 40 and 49% and increased the excretion of ¹⁴CO₂ by 96%. Addition of CA to the perfusate had no effect. Thus, CO₂ exchange is not significantly limited by pulmonary CA if inhibitors are absent. Tissue binding of [³H]acetazolamide injected into the pulmonary artery was diminished by 50% when acetazolamide concentrations reached 0.13 x 10^-6 M. Each liter of extravascular lung water contained 1.25 x 10^-6 mol of receptors for acetazolamide that were accessible to plasma during a single circulation. Binding of [³H]acetazolamide was also observed in lungs of anesthetized rabbits, suggesting that pulmonary CA is accessible to plasma in vivo as well as in situ.