PHYSIOLOGICAL CHARACTERIZATION OF PULMONARY CARBONIC-ANHYDRASE IN THETURTLE

Direct measurements have found that ectothermic vertebrates possess a significant postcapillary P-CO2 disequilibrium between arterial blood and alveolar gas, indicating that the CO2-HCO3--H+ system does not rea ch equilibrium during pulmonary capillary transit. One plausible expla nation for the blood disequilibrium is that turtle lungs lack vascular carbonic anhydrase (CA) to enhance the conversion of blood HCO3- to C O2. The present study characterized the contribution of pulmonary vasc ular CA to CO2 excretion and postcapillary CO2-HCO3--H+ equilibration in the turtle. In situ perfusion of turtle lungs with salines containi ng membrane-permeating and membrane-impermeant CA inhibitors produced significant and comparable postcapillary pH and P-CO2 perfusate disequ ilibria. Replacement of perfusate chloride with various anions had no affect on pulmonary CO2 excretion, thereby ruling out a significant co ntribution of Cl- sensitive CA isozymes (i.e., CA II-like). Perfusion of lungs with control salines following treatment with phosphatidylino sitol specific-phospholipase C produced significant CO2 disequilibria, consistent with connection of CA IV to the luminal membrane of endoth elial cells via a phosphatidylinositol glycan linkage. Vascular CA IV in the turtle lung would participate in diffusive and reactive CO2 equ ilibration and, thus, may compensate for the slow rate of the physiolo gical anion shift in turtle erythrocytes (Stabenau et al., 1991) durin g capillary transit.