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

We demonstrated pulmonary arteriolar blood flow-mediated CO gas excretion in rabbit lungs. The shear stress stimulation produced CO gas in cultured human endothelial cells of pulmonary arterioles via the activation of F/F 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 pressure (PetCO), maximal flow velocity in the pulmonary artery (Max Vp), the inner diameter (ID) of pulmonary artery, pulmonary arterial CO pressure (P mix v CO), pulmonary arterial O pressure (P mix v O), hematocrit (Hct), pH, the concentration of HCO, 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 were investigated in the human subjects. An approximately linear relationship between the PetCO and Max Vp was observed. The pumping out of 100% BV produced little or no change in the Hct, pH, P mix v CO, and P mix v O, respectively. The hemodilution produced by intravenous infusion of PSS caused a significant decrease in the Hct, but not in the PetCO. In conclusion, another route of CO gas excretion, independent of red blood cells, may be involved in human lungs.