• M Mochizuki, H Tazawa, K Niizeki, and M Tamura.
• Jpn. J. Physiol. 1981 Jan 1; 31 (3): 345-55.

AbstractWhen mixed venous blood is oxygenated in alveolar air with higher PCO2, the PCO2 within the red cell is though to exceed the alveolar PCO2 due to the Haldane effect and to block the inward CO2 diffusion. If the direction of the CO2 diffusion is not reversed during the contact time, the HCO2-gain in the plasma will not exceed the amount estimated from venoalveolar PCO2 difference by using a CO2 dissociation curve of separated plasma. In order to clarify the validity of the above thought, the venoarterial CO2 content difference was measured by using a van Slyke apparatus and a PCO2 electrode at various alveolar PCO2 levels in rebreathing dogs. The HCO3-rise in the whole blood was obviously reduced when acute hypercapnia was administered in both normoxia and hyperoxia. Quantitatively, the decrease of CO2 content under hypercapnia corresponded to the difference in CO2 content between the true and separated plasma. The reduction, however, was slightly stronger in normoxia than in hyperoxia with alveolar PO2 of 300 to 420 mmHg. These data seem to support the following explanation: When venous blood was oxygenated in normoxic air with PCO2 higher than true venous, the inward CO2 diffusion was inhibited by the Haldane effect and the reversed diffusion after the oxygenation could also be disregarded during the contact time. Because the oxygenation was accelerated in hyperoxia and the direction of the CO2 diffusion was reversed earlier than in normoxia, the plasma CO2 content became higher in hyperoxia than in normoxia.

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