Respiratory alkalosis and hypokalemia in dogs exposed to simulated high altitude

1962 ◽  
Vol 202 (6) ◽  
pp. 1041-1044 ◽  
Author(s):  
D. C. Smith ◽  
J. Q. Barry ◽  
A. J. Gold
Keyword(s):  
High Altitude ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Respiratory Alkalosis ◽  
Simulated Altitude ◽  
Simulated High Altitude ◽  
Anesthetized Dogs ◽  
Per Se ◽  
Decompression Stress

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.

Relationship of hepatic potassium efflux to phosphorylase activation induced by glucagon

1964 ◽  
Vol 206 (4) ◽  
pp. 738-742 ◽  
Author(s):  
Anthony G. Finder ◽  
Theodore Boyme ◽  
William C. Shoemaker
Keyword(s):  
Time Course ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Potassium Efflux ◽  
Blood Samples ◽  
Potassium Release ◽  
Anesthetized Dogs ◽  
Relationship Of ◽  
Primary Action ◽  
Made In

Hepatic biopsies were obtained from intact, anesthetized dogs before and at 6- to 15-sec intervals after intravenous administration of glucagon. Simultaneously, blood samples were taken from the hepatic vein at 3-sec intervals and the plasma potassium concentration measured. The time course of phosphorylase activation in hepatic biopsies was observed and compared with the time course of potassium release into the hepatic efflux. Measurements were made in normothermic (38 C) animals and in animals subjected to hypothermia (21–25 C). Maximum phosphorylase activation was reached in an average of 79 sec in normothermia and in 144 sec in hypothermia. Maximum hepatic venous potassium concentrations were observed in an average of 41 sec in normothermia and 108 sec in hypothermia. The increased hepatic potassium release which preceded the activation of phosphorylase suggested that electrolyte shifts may be involved in the primary action of glucagon upon hepatic glycogenolytic systems.

Regulation of extracellular potassium in hypothermia

1963 ◽  
Vol 205 (6) ◽  
pp. 1285-1289 ◽  
Author(s):  
G. S. Kanter
Keyword(s):  
Renal Function ◽  
Renal Tubule ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Extracellular Ph ◽  
Extracellular Potassium ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Intracellular Metabolism ◽  
K Concentration

Reduction of rectal temperature by ice packing in anesthetized dogs resulted in a fall in plasma potassium concentration in spite of the fall in arterial pH. Such a decrease in extracellular pH in normothermia would cause an increase in plasma K concentration. It was suggested that due to previously shown depression of renal acidification mechanisms in hypothermia, there occurred a K+ for Na+ exchange in the renal tubule with K+ being excreted instead of H+. It was expected that removal of renal function during hypothermia would allow the alteration in pH to cause an increase in extracellular K. Renal function was therefore removed by bilateral nephrectomy in five dogs and by ligation of both ureters in four dogs. Contrary to expectations, it was found that in the absence of renal function during hypothermia plasma K still fell markedly. No difference was found in the nephrectomized or ureter-tied dogs. It was proposed that in hypothermia, in the absence of renal function, some function of intracellular metabolism controlled extracellular K. Possibly intracellular pH decreased relatively more than did extracellular pH with a resultant movement of H+ out of the cell and K+ in. With renal function present in hypothermia, the influx of K into the cell seen in nephrectomized and ureter-tied dogs is reversed by the renal gradient which causes both a decrease in cellular and extracellular K.

Early effect of moderate altitude stress on plasma potassium in the dog

1960 ◽  
Vol 15 (1) ◽  
pp. 37-39
Author(s):  
Armand J. Gold ◽  
Jeanne Q. Barry ◽  
Frederick P. Ferguson
Keyword(s):  
Initial Level ◽  
Plasma Potassium ◽  
Respiratory Alkalosis ◽  
Moderate Altitude ◽  
Human Beings ◽  
Simulated Altitude ◽  
Maximal Level ◽  
Early Effect ◽  
Blood Ph ◽  
Partial Compensation

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

Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog

1984 ◽  
Vol 62 (9) ◽  
pp. 1129-1135 ◽  
Author(s):  
André Gougoux ◽  
Patrick Vinay ◽  
Manuel Cardoso ◽  
Marcelle Duplain
Keyword(s):  
Lactate Concentration ◽  
Plasma Potassium ◽  
Respiratory Alkalosis ◽  
Ion Concentration ◽  
Ammonia Production ◽  
Glutamine Concentration ◽  
Renal Handling ◽  
Renal Metabolism ◽  
Hydrogen Ion Concentration ◽  
Anesthetized Dogs

Acute respiratory alkalosis (blood pH, 7.60; arterial [Formula: see text], 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and ammonia production expressed per 100 mL of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma potassium concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64 to 0.38 mM during hypocapnia while α-ketoglutarate, glutamate, malate, oxaloacetate, and citrate did not change. Lactate concentration rose from 1.1 to 2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. Our data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the hydrogen ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Consequently, renal glutamine extraction and ammonia production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.

Acid-base alterations and plasma potassium concentration

1959 ◽  
Vol 197 (2) ◽  
pp. 319-326 ◽  
Author(s):  
Daniel H. Simmons ◽  
Melvin Avedon
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Alveolar Ventilation ◽  
Acid Base ◽  
Blood Ph ◽  
Arterial Ph ◽  
Significant Difference ◽  
Anesthetized Dogs ◽  
K Concentration

Arterial pH of anesthetized dogs was held constant during infusion of HCl or NaHCO3 by appropriate alterations in alveolar ventilation. While plasma potassium concentration dropped somewhat (presumably due to gradual potassium depletion), there was no significant difference in plasma potassium during the two types of infusions. The implication is that metabolic and respiratory acid-base disturbances having comparable effects on pH also have similar effects on the plasma potassium concentration. Other data support this conclusion and also indicate that effects of acidosis and alkalosis are quantitatively similar. On the basis of data of this study and of other data in the literature, it appears that the ratio of change in potassium concentration to change in blood pH ordinarily averages –3.0 to –5.0 in a steady state and that achieving a steady state requires 1–2 hours of equilibration. Data are presented which support the concept that extracellular K concentration, rather than total extracellular K, is physiologically regulated and that this involves rapid exchanges with intracellular K.

Stimulation of renin secretion by vasoactive intestinal peptide

1982 ◽  
Vol 243 (3) ◽  
pp. F306-F310
Author(s):  
J. P. Porter ◽  
I. A. Reid ◽  
S. I. Said ◽  
W. F. Ganong
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Vasoactive Intestinal Peptide ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Renin Secretion ◽  
Threefold Increase ◽  
Anesthetized Dogs ◽  
Stimulation Of

Vasoactive intestinal peptide (VIP) increased plasma renin activity (PRA) in pentobarbital-anesthetized dogs. A 15-min infusion of VIP directly into the renal artery at a dose of 33 ng . kg-1 min-1 increased renin secretion rate from 1,461 +/- 393 to 5,769 +/- 1,794 ng ANG I . ml-1 . 3 h-1 . min-1, and increased PRA from 19.2 +/- 2.3 to 29.2 +/- 4.7 ng ANG I . ml-1 . 3 h-1. Renal blood flow and creatinine clearance were also increased, whereas plasma potassium concentration and diastolic blood pressure decreased. There was no change in sodium or potassium excretion. When administered intravenously, 33 and 13 ng . kg-1 . min-1 VIP increased PRA. A dose of 3.3 ng . kg-1 . min-1 failed to increased PRA when given intravenously but produced a significant increase in PRA from 22.8 +/- 8.1 to 40.5 +/- 19.4 ng ANG I . ml-1 . 3 h-1 when infused into the renal artery. This increase occurred without any change in plasma potassium concentration or blood pressure. Renin secretion was increased by a two- to threefold increase in plasma VIP; comparable increases in plasma VIP have been reported to be produced by various experimental procedures. The data indicate that VIP increases renin secretion. The peptide appears to act directly on the kidney and may act directly on the juxtaglomerular cells.

Influence of hematocrit ratio on survival of unacclimatized dogs at simulated high altitude

1963 ◽  
Vol 205 (6) ◽  
pp. 1172-1174 ◽  
Author(s):  
Elvin E. Smith ◽  
Jack W. Crowell
Keyword(s):  
High Altitude ◽  
Carrying Capacity ◽  
Simulated Altitude ◽  
High Altitudes ◽  
Survival Group ◽  
Closed Chamber ◽  
Atmospheric Air ◽  
Simulated High Altitude ◽  
Nitrogen Ratio ◽  
Oxygen Carrying Capacity

Eighty-six dogs were subjected to acutely induced, simulated high altitudes to determine the optimum hematocrit ratio for survival. High altitudes were simulated by diluting atmospheric air with nitrogen. Dogs with various hematocrit ratios were obtained by natural selection, hemorrhage, transfusion, and pretreatment with phenylhydrazine. Fifty-one dogs, in groups of 5–15, were placed in a closed chamber, and a 40,000-ft altitude was simulated by proper adjustment of the oxygen-to-nitrogen ratio. This altitude was maintained for a period of 6 hr. Most dogs with hematocrits less than 24 or greater than 66 died before the simulated altitude of 40,000 ft was attained; those with hematocrits of 24–30 survived from 1/2 to 5 hr. Some dogs with hematocrits of 30–65 survived the entire 7-hr period. However, no dogs with hematocrits from 37 to 54 died. The same procedures were repeated at a simulated altitude of 50,000 ft with a group of 38 dogs. The survival group was composed of dogs with hematocrits of 36–46. Dogs with hematocrits of 40–41 were conscious and active while those with hematocrits on either side of this value were comatose. These data indicate that the optimum hematocrit for survival of the unacclimatized dog at acutely induced high altitude is about 40. Deaths occurring on both sides of the optimum value may be explained by a simultaneous consideration of the curves depicting oxygen-carrying capacity of the blood, and blood viscosity, at all ranges of hematocrit.

Relation of respiratory alkalosis to hypokalemia in anesthetized dogs during altitude stress

1961 ◽  
Vol 16 (5) ◽  
pp. 837-838 ◽  
Author(s):  
Armand J. Gold ◽  
Jeanne Q. Barry ◽  
Frederick P. Ferguson
Keyword(s):  
Respiratory Alkalosis ◽  
Secondary Response ◽  
Potassium Ions ◽  
Moderate Altitude ◽  
Simulated Altitude ◽  
Marked Rise ◽  
Arterial Blood ◽  
Blood Ph ◽  
Anesthetized Dogs ◽  
The Mean

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

Effect of plasma [K+] on the DC potential and on ion distributions between CSF and blood

1975 ◽  
Vol 39 (6) ◽  
pp. 1012-1016 ◽  
Author(s):  
S. W. Bledsoe ◽  
A. H. Mines
Keyword(s):  
Potassium Concentration ◽  
Electrical Potential ◽  
Fold Increase ◽  
Plasma Potassium ◽  
Electrical Potential Difference ◽  
Control Value ◽  
Ion Distributions ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Effective Role

Keeping the arterial pH at 7.4 and PaCO2 at 40 mmHg in eight anesthetized dogs, we acutely raised plasma potassium concentration from 3.4 to 8.2 meq/1, then allowed it to decay back to control levels. The cerebrospinal fluid (CSF)-blood electrical potential difference (pd) increased 13.2 mV per 10-fold increase in plasma [K+]. Again keeping arterial pH at 7.4 and PaCO2 at 40 mmHg, we elevated plasma [K+] in four dogs from 3.3 to 8.0 meq/1 and maintained this level for 6 h. We found 1) that the PD increased from a control value of +1.3 to +8.9mV, showing no tendency to decay over the 6 h; and 2) that the change in PD did not affect the distribution of Na+, K+, H+, Cl-, or HCO3- between blood and CSF over the 6 h. These results suggest that under these conditions the PD between CSF and blood may play no effective role in determining the distributions of these charged species by 6 h. These results are contrasted with recent findings which suggest that H+ and HCO3- are distributed according to passive forces between CSF and blood.

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