Studies on the localization of pulmonary carbonic anhydrase in the cat.

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Abstract
A study was made considering whether some of the carbonic anhydrase of the lung is on the surface of the pulmonary capillaries so that it acts directly on plasma as it traverses the pulmonary capillaries to accelerate CO2/pH equilibration. Experiments were performed on spontaneously breathing cats or saline-perfused cat lungs. In intact cats Tris buffer injected suddenly into the right atrium transiently lowered end-tidal CO2 [FET,CO2]. The rate of CO2 uptake came within an order of magnitude of taxing the calculated diffusing capacity of the lungs. The fall in FET,CO2 was much reduced by giving the carbonic anhydrase inhibitors benzolamide or acetazolamide i.v. or by adding benzolamide to the injected Tris. The fall in FET,CO2 could be increased by adding carbonic anhydrase to the injected Tris. In saline-perfused lungs ventilated with 5% CO2 in O2. Tris or alkalinized albumin solution injected into the pulmonary artery transiently lowered FET,CO2 and the effect was reduced by the addition of benzolamide or acetazolamide to the injectate. Injecting Tris bubbled with 15% CO2 caused a rise in FET,CO2, also reduced by benzolamide. Pulmonary carbonic anhydrase is readily accessible to large or small MW buffers in the capillaries and to inhibitors. Apparently it is located on the luminal surface of the capillary endothelium.