Summary

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 PCO₂. 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 PCO₂ 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 PCO₂, 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 PCO₂ pH and [HCO₃-] levels approaching but rarely reaching the pre-exposure values.