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Previous studies have demonstrated that elevation of arterial pCO2 is associated with an increase in the amount of pressure required to inflate the lungs. These studies do not clearly indicate whether this increase in resistance is due to a change in non-elastic or elastic resistance of the lung. In the current study, dogs were anesthetized with chloralose, and a tracheostomy and a midline sternotomy were performed. Respiration was maintained with a Starling pump. Flow, volume, and airway pressures were recorded. The dogs were respired on varying concentrations of carbon dioxide and on air. Resistance was calculated at the same flow rate and lung volume for each of the experimental conditions. In ten dogs it was demonstrated that non-elastic resistance increased in a linear fashion as the level of arterial pCO2 was raised over the range of 25 to 80 mm. Hg. Elastic resistance was unchanged. Atropine given intravenously prevented the increase in airway resistance associated with hypercapnia. The level of non-elastic resistance for any given pCOz did not change over a fifteen-minute period. The clinical implications of this observation are many, and further studies are in progress to determine whether or not similar changes occur with more prolonged periods of hypercapnia.