The effects of exogenous extracellular carbonic anhydrase on CO2 excretionin rainbow trout (Oncorhynchus mykiss): role of plasma buffering capacity

The buffering capacity (beta) of rainbow trout (Oncorhynchus mykiss) plasma was manipulated prior to intravascular injection of bovine carbonic anhydr ase to test the idea that proton (H+) availability limits the catalysed deh ydration of HCO3- within the extracellular compartment. An extracorporeal b lood shunt was employed to continuously monitor blood gases in vivo in fish exhibiting normal plasma beta (-3.9 +/- 0.3 mmol l(-1) pH unit(-1)), and i n fish with experimentally (using N-[2-hydroxyethyl]piperazine-N'-[2-ethane sulfonic acid]) elevated plasma beta (-12.1 +/- 1.1 mmol l(-1) pH unit(-1)) . An injection of 5 mg kg(-1) carbonic anhydrase equally reduced (after 90 min) the arterial partial pressure Of CO2 in trout with regular (-0.23 +/- 0.05 Torr) or high (-0.20 +/- 0.05 Torr) plasma beta; saline injection was without effect. Because ventilation and venous blood gases were unaffected by carbonic anhydrase, the effect of extracellular carbonic anhydrase in lo wering arterial partial pressure of CO2 was likely caused solely by a speci fic enhancement Of CO2 excretion owing to acceleration of HCO3- dehydration within the plasma. The lowering of arterial partial pressure of CO2 in tro ut after injection of exogenous carbonic anhydrase provides the first in vi vo evidence that the accessibility of plasma HCO3- to red blood cell carbon ic anhydrase constrains CO2 excretion under resting conditions. Because the velocity of red blood cell Cl-/HCO3- exchange governs HCO3- accessibility to red blood cell carbonic anhydrase, the present study also provides evide nce that CO2 excretion at rest is limited by the relatively slow rate of Cl -/HCO3- exchange. The effect of carbonic anhydrase in lowering arterial par tial pressure Of CO2 was unrelated to plasma buffering capacity. While thes e data could suggest that H+ availability does not limit extracellular HCO3 - dehydration in vivo at resting rates Of CO2 excretion, it is more likely that the degree to which plasma beta was elevated in the present study was insufficient to drive a substantially increased component of HCO3- dehydrat ion through the plasma.