A COMPARISON OF THE RESPONSE OF THE ANESTHETIZED DOG TO LOWERED ALVEOLAR OXYGEN DURING UNIFORM ARTIFICIAL VENTILATION AND DURING NORMALLY CONTROLLED VENTILATION

Abstract

Gaseous mixtures low in O2 were administered to dogs under morphine-urethane anesthesia. Subsequently room air was given. O2 consumption increased during the period of lowered alveolar O2 and during the subsequent period of recovery. CO2 elimination and the expiratory quotient increased during low Os and decreased below normal during recovery. Lactic acid increased slightly during the low O2 and returned toward normal during the administration of room air. The blood became very alkaline during low O2 and somewhat more acid than normal on return to room air. In 2 exps. out of 3 to determine the distribution of lactic acid, during administration of room air, the lactic acid content was highest in muscle, lowest in the testicle, and second lowest in the red blood cell. Plasma and blood concentrations were variable. During the lack of O2 there was a differential increase in lactic acid. Beginning with the highest the new order of conc. was plasma, muscle, whole blood, red blood cell, and testicle. An analysis of these results and a comparison with constant artificial ventilation exps. indicate that excess energy is required for adjusting the animal to, and for recovery from, low O2. Assuming a uniform aerobic and anaerobic metabolism and volume flow of blood throughout the body, an approximate computation indicates a decrease in the gross cH of the tissues as a result of a lowering of CO2 pressure which more than compensates for the reduction of bicarbonate base by the accumulation of fixed acid. It is suggested that oxidations are supported during lowered alveolar O2 by an accumulation of oxidizable material such as lactic acid and by a general reduction in cH of the tissues. Assuming an acid mechanism of control it is necessary to conclude that the tissues as a whole were turned more alkaline than normal during lowered alveolar O2 by virtue of an increase in the cH of some portion of the respiratory neurone chain controlling ventilation. The present exps. do not indicate which of several chemical changes resulting from lowered alveolar O2 are responsible for augmented ventilation.