THE INFLUENCE OF DENITROGENATION ON THE RESPONSE OF ANESTHETIZED DOGS TO INTRAVENOUSLY INJECTED OXYGEN

Abstract

The observations of others that O2 administered intraven, to dogs at rates from 1 ml./kg./min. rapidly produced marked increases in respiratory rates and often > 25% decreases in arterial O2 content were confirmed. Prior to the admn. of intraven. O2, animals were denitrogen-ated in order to reduce the incidence of intravascular bubble formation. In tracheotomized, anesthetized dogs denitrogen-ated by exposure to 99.6% O2 for 3-4 hr., the intraven. injn. of O2 at a rate of 1 ml./kg./min. for 20-min. periods usually produced drops in arterial O2 content, frequently of the magnitude of 5 vol. %, although occasionally there occurred slight increases. In dogs, first denitrogenated and then renitrogenated by breathing air, intraven. admn. of O2 at the same rates as previously used usually produced a rapid, significant drop in arterial O2 satn., and, in some cases, death. In contrast to the results obtained on injn. of O2 during the simultaneous admn. of intratracheal 99.6% O2, the intraven. injn. of air under similar conditions produced a rapid, extensive drop in arterial O2 satn. both before and after considerable lowering of venous N2 content had been achieved, despite the marked hyperventilation which occurred. The intraven. injn. of O2 for 180 min. at very slow rates (0.082-0.345 ml./kg./min.) in deeply anesthetized and anoxemic dogs breathing air also resulted in a continued drop of the arterial and venous O2 satn., although the amt. of O2 administered represented but 1.9-7.4% of the basal requirement. Because of the physiologic and physical factors involved in bubble formation, successful extra-pulmonic oxygenation may require some technique by which O2 can be introduced into the blood without the formation of bubbles. Even with denitrogenation and simultaneous intratracheal O2, intraven. O2 constitutes an added hazard rather than a therapeutic aid in the anoxemic state.