Effros R M, Shapiro L, Silverman P
J Appl Physiol Respir Environ Exerc Physiol. 1980 Oct;49(4):589-600. doi: 10.1152/jappl.1980.49.4.589.
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.
在灌注不含碳酸酐酶（CA）溶液的兔肺中研究了肺碳酸酐酶活性。在向肺动脉注射H¹⁴CO₃⁻、¹⁴CO₂或二者20:1的混合物后，测量呼出气体中出现的¹⁴CO₂量。与混合物相比，¹⁴CO₂在呼出气体中注入标记物的比例仅高17%，这表明在毛细血管通过时间内，H¹⁴CO₃⁻与¹⁴CO₂之间的平衡几乎完全。抑制肺CA可使H¹⁴CO₃⁻和混合物的排泄分别减少40%和49%，并使¹⁴CO₂的排泄增加96%。向灌注液中添加CA没有影响。因此，如果没有抑制剂，CO₂交换不会受到肺CA的显著限制。当乙酰唑胺浓度达到0.13×10⁻⁶M时，注入肺动脉的[³H]乙酰唑胺的组织结合减少50%。每升血管外肺水含有1.25×10⁻⁶mol乙酰唑胺受体，在单次循环中血浆可接触到这些受体。在麻醉兔的肺中也观察到了[³H]乙酰唑胺的结合，这表明肺CA在体内和原位均可被血浆接触到。
