RESPIRATORY EFFECTS OF DIETHYL ETHER IN THE CAT

¹ Departments of Anesthesiology and Pharmacology, College of Physicians and Surgeons, Columbia University, and the Anesthesiology Service, The Presbyterian Hospital, New York, N. Y.

The effect of diethyl ether on respiration was studied in decerebrate cats. Three percent ether caused no change in respiration. Five percent ether either caused no change or increased the respiratory rate and minute volume. However, ether at these concentrations decreased the ventilatory response to inhaled CO₂. Ten to 20% ether increased the respiratory rate for the first few minutes. Abolition of this effect by vagotomy shows that it is mediated through sensitization of pulmonary receptors, as previously proposed. Continued ether inhalation progressively decreased the respiratory rate, tidal volume, and minute volume. After prolonged inhalation, a secondary tachypnea was observed in association with marked respiratory acidosis. Vagotomy did not influence this response. Controlled respiration during ether inhalation prevented the development of both acidosis and the secondary tachypnea. Therefore, the late tachypnea is probably not the result of stimulation of pulmonary or extrapulmonary receptors but is a response to respiratory acidosis. The respiratory depressant effect of ether can best be explained on the basis of central depression, as demonstrated by the elevated stimulus threshold and the decreased magnitude of inspiratory shift to stimulation of the meduallry inspiratory center. With concentrations of ether up to 20%, the neuromuscular blocking action of this agent was not demonstrated at the phrenic nerve-diaphragmatic junction as studied in situ and is probably not a factor in the observed respiratory depression under these circumstances.