Physiological characterization of pulmonary carbonic anhydrase in the turtle

Abstract

Direct measurements have found that ectothermic vertebrates possess a significant postcapillary P CO 2 disequilibrium between arterial blood and alveolar gas, indicating that the CO 2-HCO − 3-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 HCO − 3 to CO 2. The present study characterized the contribution of pulmonary vascular CA to CO 2 excretion and postcapillary CO 2-HCO − 3-H + equilibration in the turtle. In situ perfusion of turtle lungs with salines containing membrane-permeating and membrane-impermeant CA inhibitors produced significant and ocmparable postcapillary pH and P CO 2 perfusate disequilibria. Replacement of perfusate chloride with various anions had no affect on pulmonary CO 2 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 CO 2 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 CO 2 equilibration and, thus, may compensate for the slow rate of the physiological anion shift in turtle erythrocytes (Stabenau et al., 1991) during capillary transit.