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