Abstract

Under certain conditions of respiratory depression, the administration of oxygen may further depress respiration or even lead to apnea and respiratory failure. It appears that in animals deeply depressed with certain anesthetics respiration may be maintained almost entirely by an anoxemic stimulus, so that oxygen by removing this stimulus depresses or abolishes respiration. Experiments on denervation and freezing of the sino-aortic mechanism indicate that administration of oxygen is equivalent to a removal of stimuli acting mainly if not entirely through this mechanism. When severe depression by oxygen is observed, the addition of carbon dioxide to the oxygen fails to prevent this depression.

Oxygen depression is more readily obtained under the same conditions in dogs than in cats. The degree of oxygen depression obtained is dependent on the anesthetic used to depress respiration. In animals given barbiturates or barbiturates plus morphine, oxygen depression is severe and easily elicited, while in animals given chlorbutanol, urethane, paraldehyde or alcohol, this effect of oxygen is slight or absent.

The difference between these two groups of anesthetics appears to lie in the fact that oxygen depression is obtained under such conditions of respiratory depression where the sino-aortic mechanism is functionally active and the response to other intrinsic or extrinsic stimuli to respiration is to a great extent eliminated.