Results of this investigation confirm the hypothesis that respiratory alkalosis is directly related to hypokalemia in dogs during their exposure to moderate altitude stress. Anesthetized animals were placed in a decompression chamber and subjected to a simulated altitude of 30,000 ft for 30 min. Arterial blood samples were obtained prior to and during the decompression period. In one series of 14 experiments in which animals breathed room air, the mean plasma K+ concentration declined from 3.9 to 3.4 mEq/ liter after 30 min. Respiratory alkalosis was demonstrated by a marked rise in blood pH (from 7.37 to 7.56) and fall in pCO2 (from 40 to 23 mm Hg) which appeared after 5 min. In a second series of 15 experiments in which dogs breathed a gas mixture containing 20% CO2 (partial pressure = 45 mm Hg at 30,000 ft), 21% O2, and 59% N2, respiratory alkalosis was effectively prevented and the characteristic hypokalemia failed to occur. It appears that potassium ions leave the plasma and enter the tissues as a secondary response to alkalosis. Submitted on March 14, 1961
Exposure of restrained, unanesthetized dogs to a simulated altitude of 30,000 ft consistently resulted in respiratory alkalosis and marked hypokalemia. When alkalosis was prevented by increasing the pCO2 of inspired air during decompression, a smaller but statistically significant decrease in plasma potassium concentration still occurred. In comparison with previous studies, the hypokalemia observed in these restrained, unanesthetized dogs was greater than that found in either unrestrained or anesthetized dogs subjected to the same decompression stress. Consequently, the suggestion is made that in the unanesthetized, restrained dog, the hypokalemic response not attributable to respiratory alkalosis is of adrenal mediation and results from the "stress" of restraint plus hyperventilation, rather than to hypoxemia or the decompression stress, per se.
Exposure of dogs to a simulated altitude of 30,000 feet for 30 minutes resulted in marked respiratory alkalosis and hypokalemia. The data failed to demonstrate, however, the appearance of the early transient hyperkalemic response which has been observed in human beings in the early moments of hyperventilation. Blood pH rose from an initial level of 7.46 to 7.71 after 3 minutes of exposure to altitude. At 30 minutes it had declined slightly from this maximal level to 7.63, suggesting the development of partial compensation to respiratory alkalosis. The results also indicated a temporal potassium-glucose relationship, potassium decreasing and glucose increasing simultaneously during exposure to altitude. Submitted on July 13, 1959
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