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Journal of Experimental Biology, Vol 202, Issue 8 965-975, Copyright © 1999 by Company of Biologists

JOURNAL ARTICLES

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

EK Stabenau and TA Heming
Department of Biology, Bradley University, Peoria, IL 61625, USA and Departments of Internal Medicine and Physiology and Biophysics, University of Texas Medical Branch, Galveston, TX 77555, USA. eks@bumail.bradley.edu.

Turtles possess a significant postcapillary CO2 partial pressure (PCO2) disequilibrium between arterial blood and alveolar gas. There are several possible explanations for this blood disequilibrium including a slow rate of erythrocyte physiological anion shift (Cl-/HCO3- exchange) or inaccessibility of plasma HCO3- to red blood cell or pulmonary carbonic anhydrase. The present study characterized the contribution of erythrocyte anion exchange and pulmonary and erythrocyte carbonic anhydrase to CO2 excretion and, hence, to postcapillary CO2-HCO3--H+ equilibration in blood-perfused turtle (Pseudemys scripta) lungs. Turtle lungs perfused in situ with red cell suspensions containing inhibitors of erythrocyte anion exchange and/or pulmonary and red cell carbonic anhydrase produced significant postcapillary blood PCO2 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 %, respectively, to CO2 excretion during single-pass perfusion, whereas red cell and pulmonary carbonic anhydrase contributed 32 % to the measured CO2 excretion. The lack of a measurable PCO2 disequilibrium during perfusion with control erythrocyte suspensions in this study suggests that alternative mechanisms may be responsible for the arterial-lung PCO2 disequilibrium measured during breathing or diving episodes in turtles.
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© The Company of Biologists Ltd 1999