Effros R M, Mason G, Silverman P
J Appl Physiol Respir Environ Exerc Physiol. 1981 Jul;51(1):190-3. doi: 10.1152/jappl.1981.51.1.190.
Pulmonary carbonic anhydrase (CA) activity was studied by injecting 0.5 ml of a buffered solution of NaH14CO3 and 3H2O into the distal airways of perfused rabbit lungs. The early recovery of 14C in the pulmonary venous outflow averaged 0.28 +/- 0.02 (SE) that of 3H under control circumstances. Incorporation of a CA inhibitor (20 mg/l acetazolamide) in the perfusate reduced 14C recovery relative to 3H by two-thirds, whereas this inhibitor had no effect when placed in the airway injection fluid. Addition of 100 mg/l Ca to the perfusate did not increase 14C recovery, but addition of the enzyme to the bronchial fluid increased 14C recovery relative to 3H by a factor of more than 5. It is concluded that CA is associated with the endothelial side of the alveolar-capillary barrier but is absent on the airway surfaces.
通过向灌注兔肺的远端气道注射0.5 ml的NaH¹⁴CO₃和³H₂O缓冲溶液,研究了肺碳酸酐酶(CA)活性。在对照情况下,肺静脉流出物中¹⁴C的早期回收率平均为³H的0.28±0.02(标准误)。灌注液中加入CA抑制剂(20 mg/l乙酰唑胺)使¹⁴C相对于³H的回收率降低了三分之二,而该抑制剂加入气道注射液时则无作用。灌注液中添加100 mg/l的Ca并未增加¹⁴C的回收率,但向支气管液中添加该酶使¹⁴C相对于³H的回收率提高了5倍多。结论是CA与肺泡-毛细血管屏障的内皮侧相关,但气道表面不存在。