The purpose of this study was to determine the effects of nitrous oxide (N2O) on the chest wall of anesthetized humans and dogs. Six human subjects and six mongrel dogs were studied during 1 minimum alveolar anesthetic concentration halothane anesthesia before and during the substitution of 70% N2O for 70% N2 in the inspired gas mixture. On a separate occasion, measurements also were made in pentobarbital-anesthetized dogs. Respiratory muscle activity was measured using electromyographic (EMG) electrodes. Chest wall configuration was determined by using fast three-dimensional computed tomography in dogs and by using respiratory impedance plethysmography in humans. N2O consistently decreased inspiratory ribcage displacement, a decrease attributable in dogs to decreased inspiratory activation of parasternal intercostal muscles; parasternal intercostal activity was not present in anesthetized humans. The decrease in ribcage motion decreased the tidal volume in humans, but not in dogs, because displacement of the diaphragm was better preserved in dogs, in association with changes in diaphragm EMG activation. N2O significantly increased phasic expiratory muscle activity in halothane-anesthetized humans and pentobarbital-anesthetized dogs. Thus, as has been demonstrated for other anesthetics, the actions of N2O are caused by alterations in the distribution and timing of neural drive to the respiratory muscles, rather than by a global depression of respiratory motoneuron drive.
Implications: In this study, we examined the effects of nitrous oxide on breathing in halothane-anesthetized dogs and humans. Nitrous oxide affected breathing by changing the distribution and timing of neural drive to the respiratory muscles in a species-dependent manner, rather than by causing a global depression of their activity.