Branchial membrane-associated carbonic anhydrase activity maintains CO2excretion in severely anemic dogfish

Abstract

Plasma CO2reactions in Pacific spiny dogfish ( Squalus acanthias) have access to plasma and gill membrane-associated carbonic anhydrase (CA). Acute severe experimental anemia and selective CA inhibitors were used to investigate the role of extracellular CA in CO2excretion. Anemia was induced by blood withdrawal coupled to volume replacement with saline. Lowering hematocrit from 14.2 ± 0.4% (mean ± SE; N = 31) to 5.2 ± 0.1% ( N = 31) had no significant impact on arterial or venous CO2tensions (PaCO2and PvCO2, respectively) over the subsequent 2 h. Pco2was maintained despite the reduction in red cell number and a significant 32% increase in cardiac output (V̇b), both of which have been found to cause PaCO2increases in teleost fish. By contrast, treatment of anemic dogfish with the CA inhibitors benzolamide (1.3 mg/kg) or F3500 (50 mg/kg), to selectively inhibit extracellular CA, elicited rapid and significant increases in PaCO2of 0.68 ± 0.17 Torr ( N = 6) and 0.53 ± 0.11 Torr ( N = 7), respectively, by 30 min after treatment. These findings provide a functional context in which extracellular CA in dogfish contributes substantially to CO2excretion. Additionally, the apparent lack of effect of V̇bchanges on Pco2suggests that, in contrast to teleost fish, CO2excretion in dogfish does not behave as a diffusion-limited system.