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.

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.

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.

Effects of sodium intake on steady-state potassium excretion

1984 ◽  
Vol 246 (6) ◽  
pp. F772-F778 ◽  
Author(s):  
D. B. Young ◽  
T. E. Jackson ◽  
U. Tipayamontri ◽  
R. C. Scott
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Concentration Data ◽  
Potassium Intake ◽  
Independent Variable ◽  
The Relationship

The effects of changes in sodium intake on the steady-state relationship between plasma potassium concentration and potassium excretion were studied in 15 chronically adrenalectomized dogs. Throughout the experiments the dogs received aldosterone at a rate of 50 micrograms/day and methylprednisolone at 1 mg/day. The relationship between plasma potassium and steady-state potassium excretion was obtained by changing potassium intake from 10 to 30 to 100 meq/day, each level being maintained for 7-10 days. At the conclusion of each period at a given level of potassium intake, plasma potassium and excretion were measured and plotted, plasma potassium being the independent variable. Such a relationship was obtained while the dogs were on three different levels of sodium intake: 10, 100, and 200 meq/day. The curves from the data obtained at 100 and 200 meq/day sodium intake both were shifted to the left of the curve obtained at 10 meq/day (P less than 0.05), although the 100 and 200 meq/day curves were not different from each other. On the basis of these data one could predict that, at a plasma potassium concentration of 4.0 meq/liter, the animals would excrete potassium at a rate of 17 meq/day on a 10 meq/day sodium intake, 37 meq/day on a 100 meq/day sodium intake, and 47 meq/day on a 200 meq/day sodium intake. Urine flow and electrolyte concentration data are consistent with the hypothesis that the sodium intake effect on potassium excretion was mediated through increases in distal nephron flow rate and decreases in distal nephron potassium concentration.

Effects of temperature on acid-base balance and ventilation in desert iguanas

1981 ◽  
Vol 51 (2) ◽  
pp. 452-460 ◽  
Author(s):  
P. E. Bickler
Keyword(s):  
Steady State ◽  
Pulmonary Ventilation ◽  
Respiratory Acidosis ◽  
Lung Ventilation ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Ph ◽  
Blood Relative ◽  
Base Balance ◽  
History Of

The effects of constant and changing temperatures on blood acid-base status and pulmonary ventilation were studied in the eurythermal lizard Dipsosaurus dorsalis. Constant temperatures between 18 and 42 degrees C maintained for 24 h or more produced arterial pH changes of -0.0145 U X degrees C-1. Arterial CO2 tension (PCO2) increased from 9.9 to 32 Torr plasma [HCO-3] and total CO2 contents remained constant at near 19 and 22 mM, respectively. Under constant temperature conditions, ventilation-gas exchange ratios (VE/MCO2 and VE/MO2) were inversely related to temperature and can adequately explain the changes in arterial PCO2 and pH. During warming and cooling between 25 and 42 degrees C arterial pH, PCO2 [HCO-3], and respiratory exchange ratios (MCO2/MO2) were similar to steady-state values. Warming and cooling each took about 2 h. During the temperature changes, rapid changes in lung ventilation following steady-state patterns were seen. Blood relative alkalinity changed slightly with steady-state or changing body temperatures, whereas calculated charge on protein histidine imidazole was closely conserved. Cooling to 17-18 degrees C resulted in a transient respiratory acidosis correlated with a decline in the ratio VE/MCO2. After 12-24 h at 17-18 degrees C, pH, PCO2, and VE returned to steady-state values. The importance of thermal history of patterns of acid-base regulation in reptiles is discussed.

scholarly journals Effects of External Acidification on the Blood Acid-Base Status and Ion Concentrations of Lamprey

1988 ◽  
Vol 136 (1) ◽  
pp. 351-361
Author(s):  
LEONA MATTSOFF ◽  
MIKKO NIKINMAA
Keyword(s):  
High Sensitivity ◽  
Co2 Concentration ◽  
Acid Base ◽  
Ion Concentrations ◽  
Ph Response ◽  
Ph Values ◽  
Blood Ph ◽  
Acid Base Status ◽  
The Difference ◽  
K Concentration

We studied the effects of acute external acidification on the acid-base status and plasma and red cell ion concentrations of lampreys. Mortality was observed within 24 h at pH5 and especially at pH4. The main reason for the high sensitivity of lampreys to acid water appears to be the large drop in blood pH: 0.6 and 0.8 units after 24 h at pH5 and pH4, respectively. The drop of plasma pH is much larger than in teleost fishes exposed to similar pH values. The difference in the plasma pH response between lampreys and teleosts probably results from the low buffering capacity of lamprey blood, since red cells cannot participate in buffering extracellular acid loads. Acidification also caused a decrease in both Na+ and C− concentrations and an elevation in K+ concentration of plasma. The drop in plasma Na+ concentration occurred faster than the drop in plasma Cl− concentration which, in turn, coincided with the decrease in total CO2 concentration of the blood.

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.

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.

Potassium loss from the heart during the immediate posthypercapnic period

1960 ◽  
Vol 198 (5) ◽  
pp. 962-964 ◽  
Author(s):  
E. B. Brown ◽  
Albert Mowlem
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Coronary Sinus ◽  
Coronary Flow ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Blood Oxygen ◽  
Blood Samples ◽  
Significant Difference ◽  
Coronary Sinus Blood

Experiments have been carried out on mongrel dogs in which plasma potassium concentrations in blood samples simultaneously drawn from the aorta and coronary sinus have been determined before, during and following 4 hours of high CO2 breathing. No significant difference between potassium concentration in aorta and coronary sinus blood was evident before or during breathing of high CO2 mixtures. Five minutes after returning to air breathing however, coronary sinus plasma potassium concentration was significantly elevated above that of the aorta. This loss of potassium from the heart is accompanied by severe cardiac irregularities, premature systoles, ventricular tachycardia and, sometimes, ventricular fibrillation. Coronary blood oxygen concentration differences decrease significantly during hypercapnia, and estimates by the N2O technique indicate that this decrease is the result of an increase in coronary flow.

Effects of acute acid-base changes on renal hemodynamics in anesthetized dogs

1965 ◽  
Vol 209 (6) ◽  
pp. 1180-1186 ◽  
Author(s):  
Daniel H. Simmons ◽  
Richard P. Olver
Keyword(s):  
Vascular Resistance ◽  
Electromagnetic Flowmeter ◽  
Respiratory Acidosis ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Acid Base ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Renal Vascular

Renal hemodynamics were studied in 58 experiments during acid-base disturbances in anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter on the left renal artery. Arterial pressure was also measured and renal vascular resistance calculated. Flow and resistance were measured during respiratory acidosis and alkalosis, metabolic acidosis and alkalosis, and combined respiratory and metabolic acid-base disturbances such that arterial pH was maintained normal while pCO2 changed. pH changes were approximately 0.2 unit above and below normal and pCO2 changed to approximately double or half control. Renal vascular resistance was shown to be pCO2 dependent but not pH dependent. Doubling the control pCO2, whether pH changed or remained constant, resulted in decreased resistance (–16%) while decreasing pCO2 to approximately one-half normal resulted in increased resistance (+17%). Resistance was not influenced by the degree of renal denervation resulting from the use of the flowmeter. Changes in resistance appear likely to be related to local rather than central factors.

Relationship between plasma potassium concentration and renal potassium excretion

1982 ◽  
Vol 242 (6) ◽  
pp. F599-F603 ◽  
Author(s):  
D. B. Young
Keyword(s):  
Renal Excretion ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Potassium Intake ◽  
Arterial Ph ◽  
The Relationship ◽  
Renal Potassium Excretion

To study the relationship between extracellular potassium concentration and renal excretion of potassium, seven chronically adrenalectomized dogs were maintained on a constant intravenous infusion of aldosterone (50 micrograms/day), and constant sodium intake (30 meq/day ) while they received four levels of potassium intake--10, 30, 100, and 200 meq/day--for 7-10 days each. At the conclusion of each level of intake, plasma potassium and renal excretion as well as other variables known to influence potassium excretion were measured. There were minimal changes in arterial pH, mean arterial pressure, extracellular fluid volume, or glomerular filtration rate at any level of potassium intake. The values for plasma potassium and renal potassium excretion attained at each level of intake were: 3.13 +/- 0.24 and 10 +/- 2; 4.18 +/- 0.18 and 21 +/- 6; 4.31 +/- 0.11 and 66 +/- 10; and 4.75 +/- 0.10 meq/liter and 170 +/- 16 meq/day, respectively. Under these experimental conditions in which the levels of aldosterone, sodium intake, arterial pH, arterial pressure, extracellular fluid volume, and glomerular filtration rate remain constant, plasma potassium concentration appears to have a week effect on renal potassium excretion below the normal level of plasma potassium (approx. 11 meq/day change in excretion for each milliequivalent per liter change in concentration). Above the normal level, however, plasma potassium concentration has a powerful effect, 260 meq/day per milliequivalent per liter. The characteristics of the relationship between plasma potassium and renal potassium excretion make it ideally suited for controlling potassium excretion in response to greater than normal potassium intake.

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