THE RÔLE OF THE ADRENAL CORTEX IN ACUTE ANOXIA 12

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Abstract
Normal men exposed to an avg. O2 tension of 98 mm. Hg. for 5 hrs. had avg. arterial O2 saturation of 83%; although O2 consumption was undiminished N excretion decreased. Exptl. animals exposed to low O2 for similar periods showed depletion of liver glycogen but no fall in blood glucose conc. unless the anoxia was extreme. Normal animals in low O2 tension for 24 hrs. suffered rises in blood glucose and liver glycogen (except in dogs), and increases in the renal excretion of N (in all animals). Adrenalectomized animals succumbed in O2 tensions that normal animals withstood, and no increase in blood glucose, liver glycogen or N excretion occurred. Treatment with "carbohydrate-regulating" factor of the adrenal cortex enabled adrenalectomized animals to withstand an otherwise fatal O2 tension, and blood glucose, liver glycogen and N excretion increased. Normal animals in low O2 tensions for 24 hrs. showed slight increases in N and P excretion and marked increases in Na, Cl and K excretion; adrenalectomized animals a striking increase in K excretion but none in N, P, Na or Cl excretion. Treatment of normal and adrenalectomized animals with "carbohydrate-regulating" factor was followed by striking increases in Na, Cl and water excretion but none in K excretion. In initial anoxia there is an increased utilization of carbohydrate; normal blood glucose conc. is maintained from liver glycogen stores. Successful adaptation to continued exposure to low O2 tension depends in part upon increase in protein catabolism with storage of carbohydrate and excretion of N; these changes do not occur without adrenal cortex. The increase in K excretion is probably related to factors other than the adrenal cortex, whereas the increase in Na and Cl excretion is mediated by the "carbohydrate-regulating" factor.