Effect of potassium depletion on cerebrospinal fluid bicarbonate homeostasis

1976 ◽  
Vol 231 (2) ◽  
pp. 579-587 ◽  
Author(s):  
EE Nattie ◽  
SM Tenney
Keyword(s):  
Potassium Depletion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mixed Acid ◽  
Base Balance ◽  
Upward Direction ◽  
Relationship Of ◽  
The Relationship ◽  
K Depletion

We have examined the effect of K depletion on CSF [HCO3-] homeostasis in awake rats. The relationship of CSF [HCO3-] to arterial [HCO3-] in metabolic acid-base disturbances is displaced is an upward direction and has a significantly increased slope in K-depleted vs. control rats (0.51 +/- 0.02 vs. 0.42 +/- 0.02). Results of partial K-repletion experiments, with peripheral acid-base balance held constant, suggest that the effect is K specific. The K-depleted animals also exhibit a wider (CSF-arterial) PCO2 difference than controls (11.1 vs. 8.4 mmHg). When CSF [HCO3-] is shown as a function of CSF PCO2 the data of K-depleted rats are no longer displaced when compared to controls but still have a significantly greater slope (1.21 +/- 0.23 vs. 0.89 +/- 0.08). This increased slope is interpreted to reflect enhanced HCO3- movement from blood to CSF at high arterial [HCO3-]. Analysis of our data and observations from the literature in conditions of mixed acid-base disturbances suggest that CSF [HCO3-] is determined by a) CSF PCO2 and b) the level of arterial [HCO3-] when the latter is greater than the normal CSF [HCO3-].

Calculation of physiological acid-base parameters in multicompartment systems with application to human blood

2003 ◽  
Vol 95 (6) ◽  
pp. 2333-2344 ◽  
Author(s):  
E. Wrenn Wooten
Keyword(s):  
Base Change ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Parameters ◽  
Present Formalism ◽  
Base Balance ◽  
Multicompartment Systems ◽  
Relationship Of ◽  
The Relationship

A general formalism for calculating parameters describing physiological acid-base balance in single compartments is extended to multicompartment systems and demonstrated for the multicompartment example of human whole blood. Expressions for total titratable base, strong ion difference, change in total titratable base, change in strong ion difference, and change in Van Slyke standard bicarbonate are derived, giving calculated values in agreement with experimental data. The equations for multicompartment systems are found to have the same mathematical interrelationships as those for single compartments, and the relationship of the present formalism to the traditional form of the Van Slyke equation is also demonstrated. The multicompartment model brings the strong ion difference theory to the same quantitative level as the base excess method.

The relationship of plasma glutamine to ammonium and of glycine to acid-base balance in propionic acidaemia

2003 ◽  
Vol 26 (1) ◽  
pp. 89-91 ◽  
Author(s):  
Z. N. Al-Hassnan ◽  
S. A. Boyadjiev ◽  
V. Praphanphoj ◽  
A. Hamosh ◽  
N. E. Braverman ◽  
...  
Keyword(s):  
Propionic Acidaemia ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Relationship Of ◽  
The Relationship

Defect in the Renal Tubular Reabsorption of Water Associated With Potassium Depletion in Rats

1957 ◽  
Vol 189 (3) ◽  
pp. 557-563 ◽  
Author(s):  
Walter Hollander ◽  
Robert W. Winters ◽  
T. Franklin Williams ◽  
John Bradley ◽  
Jean Oliver ◽  
...  
Keyword(s):  
Urinary Concentration ◽  
Potassium Depletion ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Tubular Reabsorption ◽  
Renal Concentrating Mechanism ◽  
Renal Tubular ◽  
Relationship Of ◽  
The Relationship ◽  
K Depletion

The effect of graded degrees of K depletion on the ability to produce a concentrated urine was studied in Sprague-Dawley rats. With increasing degrees of K depletion, as measured by the concentration of K in fat-free skeletal muscle, there was a progrossive decrease in the maximum urinary concentration. This defect of the renal concentrating mechanism appeared to be better correlated with the degree than with the duration of potassium depletion and could be demonstrated either by the use of exogenous vasopressin or by water deprivation. The potassium-deficient rats in at least one experiment developed a significant polydipsia. The data do not allow any conclusions with respect to the relationship of the polydipsia to the renal concentrating defect except that the latter at least was not severe at the onset of the increased water intake.

Effects of potassium and rubidium on muscle cell bicarbonate

1962 ◽  
Vol 203 (1) ◽  
pp. 209-214 ◽  
Author(s):  
James B. Hudson ◽  
Arnold S. Relman
Keyword(s):  
Skeletal Muscle ◽  
Intraperitoneal Injection ◽  
Renal Cortex ◽  
Acid Base Balance ◽  
Acid Base ◽  
Sharp Rise ◽  
Extracellular Acidosis ◽  
Rapid Exchange ◽  
Base Balance ◽  
K Depletion

A tissue CO2 content method was used to study the effects of Rb and K on skeletal muscle bicarbonate and pH in rats. Intraperitoneal injection of large loads of RbCl or KCl in normal rats produced extracellular acidosis and a transient intracellular alkalosis in muscle (and also in renal cortex). This supports previous suggestions that rapid exchange of administered cation for intracellular hydrogen occurs. In K-deficient alkalotic rats, loading with RbCl or KCl caused a greater fall in extracellular bicarbonate but a smaller rise in muscle bicarbonate. Muscle bicarbonate was unchanged by the alkalosis of K depletion or the reduction in extracellular bicarbonate resulting from chronic feeding of Rb. After the acute RbCl and KCl loads, repair of intracellular alkalosis occurred within 6 hr, associated with a transient sharp rise in tissue citrate content. It is suggested that production of citrate and other metabolic acids may play a role in stabilizing cellular acid-base balance.

scholarly journals Ventilation and acid-base balance during graded activity in lizards

1981 ◽  
Vol 240 (1) ◽  
pp. R29-R37 ◽  
Author(s):  
G. S. Mitchell ◽  
T. T. Gleeson ◽  
A. F. Bennett
Keyword(s):  
Treadmill Exercise ◽  
Control Level ◽  
Hydrogen Ion ◽  
Co2 Production ◽  
Acid Base Balance ◽  
Acid Base ◽  
Lizard Species ◽  
Arterial Pco2 ◽  
Base Balance ◽  
Graded Activity

Arterial PCO2, hydrogen ion ([H+]a), and lactate ([L]a) concentrations, rates of metabolic CO2 production (VCO2) and O2 consumption (VO2), and effective alveolar ventilation (Veff) were determined in the lizards Varanus exanthematicus and Iguana iguana at rest and during steady-state treadmill exercise at 35 degrees C. In Varanus, VCO2 increased ninefold and VO2 sixfold without detectable rise in [L]a at running speeds below 1.0 to 1.5 km x h-1. In this range, Veff increased 12-fold resulting in decreased levels of PaCO2 and [H+]a. At higher speeds [L]a rose. Increments of 5 mM [L]a were accompanied by hyperventilation, reducing PaCO2 and thus maintaining [H+]a near its resting level. When [L]a increased further, [H+]a increased. Sustainable running speeds (0.3-0.5 km x h-1 and below) were often associated with increased VO2, VCO2, and [L]a in Iguana. Sixfold increases in VCO2 and 9-mM increments in [L]a were accompanied by sufficient increase in Veff (9-fold) to maintain [H+]a at or below its control level. When [L]a increased further, [H+]a increased. These results indicate that both lizard species maintain blood acid-base homeostasis rather effectively via ventilatory adjustments at moderate exercise intensities.

Effect of chronic acetazolamide administration on gas exchange and acid-base control after maximal exercise

1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Gas Exchange ◽  
Muscle Power ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Co2 Output ◽  
Base Balance ◽  
Arterial Plasma

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)

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