ABSTRACT
An abrupt increase in ambient CO2 resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the
of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood
during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with
pH and [HCO3−] levels approaching but rarely reaching the pre-exposure values.