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 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.
D000086:Acetazolamide / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001665:Binding Sites; D001834:Body Water / Q000378:metabolism; D002245:Carbon Dioxide / Q000502:physiology*; D002257:Carbonic Anhydrase Inhibitors / Q000378:metabolism; D002256:Carbonic Anhydrases / Q000378:metabolism*; D008168:Lung / Q000201:enzymology*; D008433:Mathematics; D010477:Perfusion; D011817:Rabbits; D012119:Respiration
D001639:Bicarbonates; D002257:Carbonic Anhydrase Inhibitors; D002245:Carbon Dioxide; D002256:Carbonic Anhydrases; D000086:Acetazolamide