Effect of a Narcotic Level of CO2 on Adrenal Cortical Activity and Carbohydrate Metabolism

Publisher Website
Google Scholar
Abstract
Normal unanesthetized guinea pigs and normal, adrenalectomized, and hypophysectomized rats were exposed to 30% CO2 in air and in O2 for a period of 1 hour, followed by a recovery period on air of 1 hour. Both gas mixtures produced a severe degree of acidosis in guinea pigs, but under 30% CO2 in air the animals also developed a superimposed hypoxia. After 1 hour exposure to 30% CO2 in air, pH fell to 6.86 and the O2 content of the blood dropped to 6.41%, compared with a pH of 6.95 and an O2 content of 11.6% after 1 hour exposure to 30% CO2 in O2. After 1 hour recovery on air following exposure to both experimental conditions the blood CO2 content remained significantly higher than the initial level. Exposure to 30% CO2 in air (CO2 plus hypoxia) produced in guinea pigs an increased adrenal cortical activity as indicated by a significant fall in adrenal cholesterol, a slight drop in circulating lymphocytes and a significant increase in adrenal weight. Blood eosinophils showed an atypical increase of 190%, while the total number of leucocytes did not change. Exposure to 30% CO2 in O2 (CO2 effect only) caused no significant changes in adrenal cholesterol, adrenal weight, in circulating lymphocytes, eosinophils, or total leucocytes in guinea pigs. Liver glycogen decreased continuously during exposure to both CO2 mixtures and blood glucose increased correspondingly, (96% and 95% respectively) at the end of 60 minutes of exposure. Muscle glycogen increased under 30% CO2 in air, probably correlated with an adrenal cortical stimulation, while lactic acid tended to decrease. An opposite change took place under 30% CO2 in O2: muscle glycogen decreased and lactic acid rose markedly. During the recovery period on air following exposure to both CO2 mixtures a strong adrenal cortical stimulation took place, as indicated by the fall of adrenal cholesterol, and lymphocytes and eosinophil counts. Liver glycogen continued to fall, while blood sugar returned to approximately initial levels. Blood sugar in normal and adrenalectomized rats increased significantly during exposure to both CO2 mixtures. After 1 hour of exposure to 30% CO2 in air, blood sugar in normal rats rose 60% while in adrenalectomized rats the increase amounted only to 30%. Under 30% CO2 in O2 the blood sugar increases in normal and adrenalectomized rats did not differ significantly (32% compared with 29%). This indicated that epinephrine release plays a role during exposure to 30% CO2 in air. Since the blood sugar response in hypophysectomized rats was even higher than in normal rats, a possible CO2 effect on the pancreatic hyperglycemic factor via the pituitary growth hormone was excluded. Plasma K and Na increased in guinea pigs during exposure to both CO2 mixtures and decreased below the initial level during the 1 hour recovery. Possible mechanisms for K and Na shifts are discussed. The continuous decrease of liver glycogen observed in guinea pigs during and following exposure to 30% CO2 in air and in O2 and blood sugar increase found in adrenalectomized rats under these conditions is in striking contrast to the effects of anoxia and suggests an inhibition of the "vago-insulin system" under high CO2 concentrations.