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The concentration of lactic acid, sodium, potassium and calcium was measured in four structures of the brain 3 hours after death in anesthetized and unanesthetized dogs which had been subjected to simulated altitude and ground level control protocols for 15 minutes. The effect of the simulated altitude was elevation of a) the sodium concentration in the corona radiata but not in the cerebral cortex or caudate nucleus, b) the calcium concentration in the cortex, corona radiata and caudate nucleus and c) the lactic acid concentration in all the tissues. No potassium changes were noted. The effect of the anesthesia was very slight and only indirectly detectable. The sampling problem was studied and caudate nucleus and cortex recommended as sampling sites for the detection of hypoxia by lactic acid elevation if a whole hemisphere cannot be used. It is pointed out that accuracy in diagnosing ante mortem hypoxia depends upon discrete anatomical sampling since lactic acid is not evenly distributed within the brain. A chemical approach to give compensation for the uneven distribution of lactic acid is presented.

The lactic acid concentration of brain was measured 3 hours after death in dogs which had been subject to hypocapnia, hypoxemia with hypocapnia, and hypoxemia without hypocapnia for 15 minutes. There was no elevation of brain lactic acid above the control level in those dogs subjected to hypocapnia or hypoxemia alone, however, when hypocapnia and hypoxemia were combined there was a significant increase. Cardiovascular and blood chemical analyses support the conclusion that variations in cerebral blood flow, availability of oxygen at the tissue level and interference with oxidative metabolism are important determining factors in brain lactic acid build-up. The results agree with those obtained in altitude-exposed animals, for they likewise show an elevation of brain lactic acid.

Blood sugar levels of 93 dogs are reported. In animals in which respiration was controlled and hypoxemia or hypocapnia induced for 15 minutes, there was no change in blood sugar. However, there was an elevation when hypocapnia and hypoxemia were combined. Exposure for 30 minutes elevated blood sugar to a greater extent in the hypoxemic group than in the combined hypocapnic and hypoxemic group, whereas hypocapnia alone produced no change. Exposure of pentobarbital sodium-injected or uninjected dogs to 30,000 feet simulated altitude for 15 minutes failed to produce a statistically significant increase in blood sugar, although evidences were observed of a physiologically important increase.

The concentration of 17-hydroxycorticosterone and a corticosterone-like fraction in peripheral venous blood was not elevated significantly following 15- or 30-minute exposure of dogs to hypocapnia induced by hyperventilation, to hypoxemia induced by breathing 5% oxygen, or to the combination of these conditions. Neither were there significant differences between control and exposed animals in ACTH content of anterior pituitary tissue, or in ascorbic acid content of adrenals. Cytological study of sections of anterior pituitaries revealed somewhat greater than normal acidophilia in all dogs, with the greatest acidophilia being observed in the hypocapnic animals. The concentration of 17-hydroxycorticosterone was higher than that of the corticosterone-like fraction, the 17-hydroxycorticosterone to corticosterone-like ratio varying from 1.3:1 to 1.7:1.