CO2 excretion and postcapillary pH equilibration in blood-perfused turtle lungs

Turtles possess a significant postcapillary CO2 partial pressure (P-CO2) di sequilibrium between arterial blood and alveolar gas. There are several pos sible explanations for this blood disequilibrium including a slow rate of e rythrocyte physiological anion shift (Cl-/HCO3- exchange) or inaccessibilit y of plasma HCO3- to red blood cell or pulmonary carbonic anhydrase. The pr esent study characterized the contribution of erythrocyte anion exchange an d pulmonary and erythrocyte carbonic anhydrase to CO2 excretion and, hence, to postcapillary CO2-HCO3--H+ equilibration in blood-perfused turtle (Pseu demys scripta) lungs. Turtle lungs perfused in situ with red cell suspensio ns containing inhibitors of erythrocyte anion exchange and/or pulmonary and red cell carbonic anhydrase produced significant postcapillary blood P-CO2 and pH disequilibria, while no disequilibria were measured when lungs were perfused with control red cell suspensions. Erythrocyte anion exchange and pulmonary intravascular carbonic anhydrase contributed 11 % and 9 %, respe ctively, to CO2 excretion during single-pass perfusion, whereas red cell an d pulmonary carbonic anhydrase contributed 32 % to the measured CO2 excreti on, The lack of a measurable P-CO2 disequilibrium during perfusion with con trol erythrocyte suspensions in this study suggests that alternative mechan isms may be responsible for the arterial-lung P-CO2 disequilibrium measured during breathing or diving episodes in turtles.