Another route of CO 2 gas excretion independent of red blood cells in human lungs.

We demonstrated pulmonary arteriolar blood flow-mediated CO ₂ gas excretion in rabbit lungs. The shear stress stimulation produced CO ₂ gas in cultured human endothelial cells of pulmonary arterioles via the activation of F ₁ /F _o ATP synthase. To confirm the findings in human subjects undergoing the operation with heart-lung machines, we aimed to evaluate the effects of a stepwise switch, from a partial to a complete cardiopulmonary bypass, of the circulatory blood volume (BV, 100% = 2.4 × cardiac index), on the end-expiratory CO ₂ pressure (PetCO ₂ ), maximal flow velocity in the pulmonary artery (Max Vp), the inner diameter (ID) of pulmonary artery, pulmonary arterial CO ₂ pressure (P mix v CO ₂ ), pulmonary arterial O ₂ pressure (P mix v O ₂ ), hematocrit (Hct), pH, the concentration of HCO ₃ ^- , and base excess (BE) in mixed venous blood in 9 patients with a mean age of 72.3 ± 3.4 years. In addition, the effects of the decrease in Hct infused with physiological saline solution (PSS) on PetCO ₂ were investigated in the human subjects. An approximately linear relationship between the PetCO ₂ and Max Vp was observed. The pumping out of 100% BV produced little or no change in the Hct, pH, P mix v CO ₂ , and P mix v O ₂ , respectively. The hemodilution produced by intravenous infusion of PSS caused a significant decrease in the Hct, but not in the PetCO ₂ . In conclusion, another route of CO ₂ gas excretion, independent of red blood cells, may be involved in human lungs.
(© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)