Physiological characterization of pulmonary carbonic anhydrase in the turtle.

Direct measurements have found that ectothermic vertebrates possess a significant postcapillary PCO2 disequilibrium between arterial blood and alveolar gas, indicating that the CO2-HCO3(-)-H+ system does not reach equilibrium during pulmonary capillary transit. One plausible explanation for the blood disequilibrium is that turtle lungs lack vascular carbonic anhydrase (CA) to enhance the conversion of blood HCO3- to CO2. The present study characterized the contribution of pulmonary vascular CA to CO2 excretion and postcapillary CO2-HCO3(-)-H+ equilibration in the turtle. In situ perfusion of turtle lungs with salines containing membrane-permeating and membrane-impermeant CA inhibitors produced significant and comparable postcapillary pH and PCO2 perfusate disequilibria. Replacement of perfusate chloride with various anions had no affect on pulmonary CO2 excretion, thereby ruling out a significant contribution of Cl- sensitive CA isozymes (i.e., CA II-like). Perfusion of lungs with control salines following treatment with phosphatidylinositol specific-phospholipase C produced significant CO2 disequilibria, consistent with connection of CA IV to the luminal membrane of endothelial cells via a phosphatidylinositol glycan linkage. Vascular CA IV in the turtle lung would participate in diffusive and reactive CO2 equilibration and, thus, may compensate for the slow rate of the physiological anion shift in turtle erythrocytes (Stabenau et al., 1991) during capillary transit.