In vivo and in vitro CO2 Buffer Curves on Rabbit and Potassium Transfer

In vivo and in vitro CO2 buffer curves for blood were determined from 29 rabbits breathing room air, 10% CO2 in air, and 20% CO, in air. In vivo blood CO2 buffer curve had a slope of 26. 5 mEq/L, pH. In vitro blood had a slope of 40. 4 mEq/L, pH and seperated plasma had a slope of 6. 4 mEq/L, pH. In order to determine the metabolic component which developes during respiratory acidosis, bicarbonate concentrations which wouJdexist at pH 7.40 were calculated. Almost all animal revealed that metabolic acidosis was superimposed on severe (20% CO, inhalation). respiratory acidosis because the plasma bicarbonate concentration during elevated CO, tensions did not attain the value it would attain from blood in equilibrium with the same CO2 tension in vitro. It did not appear that much of this "bicarbonate deficit" was due simply to the fact that the in vivo CO, blood buffer curve had a lower slope than in vitro curve and in vivo blood has much greater distribution space of additional bicarbonate, formed with increased CO, tension through interstitium. Average bicarbonate deficit of approximately 6.4 mEq/L was present when arterial PC0 2 had risen more than 100 mmHg in an hour. Plasma potassium concentration was compared before and during 10%, 20% CO2 breathing. Rabbits regularly showed an increase in plasma potassium concentration during breathing of 20% CO2 mixture, Especially, immediately following returning to room air breathing, there was a further rise in this concentration. This tendency was more marked in the rabbits exposed to high CO2 for a prolonged period. Although quantitative analysis for the relationship between each plasma hydrogen ion concentration and the potassium failed, the pattern of changes in plasma potassium before and during hypercapnia was highly significant