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The classical concept of CO₂ gas exchange in the lungs is well established [1]. Thus, the first step in CO₂ gas exchange involves a combination of the physiological processes required for CO₂ gas diffusion from cells in tissues, the catalysis of carbonic acid dehydration, and transmembrane HCO₃^- -Cl^- exchange in red blood cells. The second step involves the oxygenation of hemoglobin and the simultaneous liberation of protons, which are then able to retract with HCO₃^- within red blood cells, resulting in the excretion of CO₂ gas from the red blood cells in the pulmonary capillaries.

Currently, with cellular, molecular, and in vivo animal experiments, the new concept of pulmonary blood flow-mediated CO₂ gas exchange in the lungs is demonstrated [2,3]. Thus, we showed that 10s shear stress stimulation induced stress strength-dependent H⁺ release followed by CO₂ gas excretion from pulmonary arteriolar endothelial cells, which was significantly reduced by the inhibition of cell surface F₁/F₀ ATP synthase or carbonic anhydrase type IV. Based on these findings, we proposed the new concept of CO₂ gas excretion in the lungs, pulmonary arteriolar flow-mediated cell surface F₁/F₀ ATP synthase-dependent H⁺ secretion, which results in the facilitation of a dehydration reaction involving HCO^- in the plasma followed by CO₂ gas excretion from the arteriolar endothelial cells. To further examine the validity of the proposed new concept, we investigated the effects of intramediastinal balloon catheterization-, pulmonary artery catheterization-, or isoprenaline-induced changes in the pulmonary blood flow on the end-expiratory CO₂ gas pressure (PECO₂), the maximal velocity of pulmonary artery (Max Vp), systemic arterial pressure of anesthetized rabbits. We also evaluated the changes in the PECO₂ in clinical model of anemia. An almost linear relationship was detected between the PECO₂ and Max Vp. When small pulmonary arteries were subjected to stenosis, the PECO₂ fell rapidly, and the speed of the reduction was dependent on the degree of stenosis. Isoprenaline produced significant increases in the PECO₂. Conversely, the treatment with a cell surface F₁/F₀ ATP synthase antibody caused significant reductions in the PECO₂ itself and isoprenaline-induced increase in the PECO₂. Neither the PECO₂ nor systemic arterial pressure was significantly influenced by marked anemia (%hematocrit, ~70%). On the other hand, in the presence of severe anemia (%hematocrit, ~100%) both the PECO₂ and the arterial pressure fell significantly when the rabbit’s blood viscosity was decreased. With these findings of in vivo animal experiments, we reaffirm the validity of the proposed new concept of CO₂ gas exchange in the lungs.

The new concept of pulmonary blood flow-mediated CO₂ gas exchange in the lungs may offer reasonable answers for several serious questions which remain still unanswered under the classical concept of CO₂ gas exchange in the lungs. For example, the physiological CO₂ gas excretion was observed in isolated rat lungs that were perfused with a red blood cell-free Krebs-Ringer bicarbonate solution [4]. Moreover, in patients with severe anemia, little or no symptoms of reduced CO₂ transport-mediated acidosis have been confirmed [5].

References

1. Klocke R (1987) Carbon dioxide transport. In: Handbook of Physiology. The Respiratory System. Gs Exchange. Bethesda MD. Am Physiol Soc 173-197.
2. Kawai Y, Yoshida K, Kaidoh M, Yokoyama Y, Ohhashi T (2012) Shear stress-mediated F1/F0 ATP synthase-dependent CO2 gas excretion from human pulmonary arteriolar endothelial cells. J Cell Physiol 227: 2059-2068. [Crossref]
3. Kawai Y, Ajima K, Kaidoh M, Sakaguchi M, Tanaka S, et al. (2015) In vivo support for the new concept of pulmonary blood flow-mediated CO2 gas excretion in the lungs. Am J Physiol Lung Cell Mol Physiol 308: L1224-1236.[Crossref]
4. Crandall ED, O'Brasky JE (1978) Direct evidence of participation of rat lung carbonic anhydrase in CO2 reactions. J Clin Invest 62: 618-622. [Crossref]
5. Glader B (2003) Anemia: General considerations. In: Wintrobe’s clinical hematology. Philadelphia, Lipponcott Williams and Wilkins 947-978.