Pulmonary Carbonic Anhydrase and the Release of Carbon Dioxide from Plasma Bicarbonate

Abstract

Although red cells contain a considerable excess of carbonic anhydrase¹, ², ³ evidence has been obtained that the enzyme is not accessible to carbonic acid in the plasma⁴. A number of investigators have hypothesized that the absence of carbonic anhydrase in the plasma is responsible for a persistent disequilibrium between bicarbonate and carbon dioxide throughout the circulation^4–9. The consequences of such disequilibrium in the pulmonary vasculature are shown in Figure 1. The passage of carbon dioxide from the plasma and red cells to alveolar gas is followed by the rapid conversion of HCO ^-₃ to CO₂ within the red cells. This reaction proceeds at a much slower rate in the plasma because the reaction is uncata1yzed in plasma. Plasma HC0 ^-₃ diffuses into the red cells in exchange for C1^- (Hamburger Shift) and then combines with the hydrogen ions within the red cell to form additional H₂C0₃ and CO₂ , Although the latter reactions result in the consumption of H⁺ within the red cells, the pH of plasma remains unchanged. Movement of both H⁺ and OH^- across the red cell membrane is reportedly very slow¹⁰ and the rate at which equilibration occurs between red cell and plasma pH appears to be limited by the uncatalyzed conversion of H₂C0₃ to CO₂ in the plasma⁴.