Because the means by which analeptics stimulate respiration is generally unknown, a study was instituted to evaluate the effect of ethamivan (Emivan) on the threshold response of the human respiratory center to carbon dioxide. Alveolar carbon dioxide tensions and minute respiratory volumes were measured in normal subiects prior to the administration of any drug, folloWing elevation of the threshold of the respiratory center to carbon dioxide produced by meperidine and thiopental, and, finally, following the intravenous IUlministration of ethamivan.The effects of ethamivan were tested only in subiects whose respiration had been depressed because of the suggested use of analeptics in such states. The results showed that in the presence of respiratory depression, ethamivan produced a prompt and significant increase in ventilation but that with the dosage tested ethamivan did not fully restore ventilation to normal control value. Ethamivan produced this effect by lowering the previously elevated threshold response of the respiratory center to carbon dioxide rather than by inducing hyperventilation through other neurophysiologic mechanisms.