The purpose of this study was to determine the effects of nitrous oxid
e (N2O) on the chest wall of anesthetized humans and dogs. Six human s
ubjects and six mongrel dogs were studied during 1 minimum alveolar an
esthetic concentration halothane anesthesia before and during the subs
titution of 70% N2O for 70% N-2 in the inspired gas mixture. On a sepa
rate occasion, measurements also were made in pentobarbital-anesthetiz
ed dogs. Respiratory muscle activity was measured using electromyograp
hic (EMG) electrodes. Chest wall configuration was determined by using
fast three-dimensional computed tomography in dogs and by using respi
ratory impedance plethysmography in humans. N2O consistently decreased
inspiratory ribcage displacement, a decrease attributable in dogs to
decreased inspiratory activation of parasternal intercostal muscles; p
arasternal 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 pre
served in dogs, in association with changes in diaphragm EMG activatio
n. N2O significantly increased phasic expiratory muscle activity in ha
lothane-anesthetized humans and pentobarbital-anesthetized dogs. Thus,
as has been demonstrated for other anesthetics, the actions of N2O ar
e caused by alterations in the distribution and timing of neural drive
to the respiratory muscles, rather than by a global depression of res
piratory motoneuron drive. Implications: In this study, we examined th
e effects of nitrous oxide on breathing in halothane-anesthetized dogs
and humans. Nitrous oxide affected breathing by changing the distribu
tion and timing of neural drive to the respiratory muscles in a specie
s-dependent manner, rather than by causing a global depression of thei
r activity.