The Journal of Experimental Medicine
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The Journal of Experimental Medicine, Vol 37, 69-81, Copyright, 1923, by The Rockefeller Institute for Medical Research New York

ARTICLE

THE ACTION OF DRUGS ON RESPIRATION : II. ETHER, CHLOROFORM, CHLORAL, URETHANE, LUMINAL, MAGNESIUM, CAFFEINE, STRYCHNINE, AND ATROPINE.



Carl F. Schmidt M.D.1 and W. Benson Harer M.D.1

1 From the Laboratory of Pharmacology of the University of Pennsylvania, Philadelphia.

1. The depressant drugs which have been studied in this series of experiments were found to resemble morphine and heroine in that they depressed expiration more than inspiration, but they acted only in narcotic doses and always depressed inspiration at the same time. Ether caused a sharp expiratory rhythm, persisting until narcosis was very deep, probably a result of irritation of the air passages. Chloroform sometimes caused dyspnea, even in very deep narcosis, probably because of circulatory depression. Hydrated chloral made respiration more rapid, but shallower. Urethane usually made expiration active, often with inspiratory pauses, such as may follow vagotomy. Magnesium seemed to produce the most uniform, uncomplicated depression of all the depressants tried. Luminal resembled morphine and heroine more closely than any of the general depressants, making expiration passive without depressing inspiration, but it acted only in narcotic doses, unlike morphine and heroine.

2. Caffeine and strychnine, whenever they caused acceleration after morphine, brought back active expiration. Atropine never stimulated, and commonly acted as a synergist to morphine.

3. It is suggested that the results outlined in this and the preceding paper point to the existence of a separate central mechanism for the control of each of the phases of respiration, and that, while each responds to the same chemical stimuli, the threshold of the expiratory is higher than that of the inspiratory. Evidence is presented to indicate that if expiration remains passive a marked increase in depth of breathing may slow the rate, and a respiratory mechanism that lacks active expiration may be so inefficient that a CO2 concentration which stimulated when expiration was active may depress when it is passive.

 Submitted on July 20, 1922


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