Effects of Metabolic Alkalosis, Metabolic Acidosis and Uraemia on Whole-Body Intracellular pH in Man

1977 ◽  
Vol 52 (2) ◽  
pp. 125-135 ◽  
Author(s):  
A. Tizianello ◽  
G. De Ferrari ◽  
G. Gurreri ◽  
N. Acquarone
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Buffer Capacity ◽  
Normal Subjects ◽  
Extracellular Ph ◽  
Whole Body ◽  
Cellular Environment ◽  
Acid Load ◽  
Acute Metabolic Acidosis

1. Whole-body intracellular pH (pH1) was measured by the 14C-labelled DMO method in twenty-four control subjects, eighteen normal subjects with induced acute metabolic alkalosis, ten normal subjects with induced acute metabolic acidosis, twelve normal subjects with chronic acidosis and in fifteen patients with chronic renal insufficiency and acidosis. 2. The change in pH1 per unit change in extracellular pH is significantly larger in acute metabolic alkalosis than in acute metabolic acidosis. In chronic metabolic acidosis, pH1 decreased in proportion to the total amount of ammonium chloride administered; pH1 was normal in patients with uraemic acidosis. 3. These observations confirm the role that tissue buffers play in the protection of the cellular environment in some forms of acidosis. When the acid load overwhelms tissue buffer capacity, pH1 becomes a function of extracellular pH. 4. Cells seem more protected from acute acidosis than from acute alkalosis.

Plasma, Extracellular and Muscle Electrolyte Responses to Acute Metabolic Acidosis

1956 ◽  
Vol 186 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Richard B. Tobin
Keyword(s):  
Metabolic Acidosis ◽  
Hydrochloric Acid ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Acid Base ◽  
Extracellular Acidosis ◽  
Acid Load ◽  
Acute Metabolic Acidosis ◽  
Volumes Of Distribution

Nephrectomized cats were infused with hydrochloric acid in loads of from 3.5–9.6 mEq/kg. Extracellular moderation of the acidosis calculated from concentrations of electrolytes in plasma and inulin volumes of distribution was proportioned as follows: 35% by Na and 5% by K entering the ECS, and 20% by Cl and 24% by CO2 leaving the ECS. Calculated from changes in the chloride spaces, Na shift moderated 58%, CO2 22% and K 6% of the acid load. Sodium rather than potassium appeared to be the main extracellular moderator of acidosis under the conditions of these experiments. Direct muscle analyses showed a fall in intracellular Na and probably of K in response to extracellular acidosis. It is suggested that K i is not inversely related to extracellular ph. Calculated intracellular ph remained constant during the acidosis, indicating that cells may maintain a constant acid-base environment despite marked fluctuations of extracellular ph and that unmeasured mechanisms are responsible.

The Effect of Simulated Metabolic Acidosis on Intracellular pH and Lactate Metabolism in the Isolated Perfused Rat Liver

1973 ◽  
Vol 45 (4) ◽  
pp. 543-549 ◽  
Author(s):  
M. H. Lloyd ◽  
R. A. Iles ◽  
B. R. Simpson ◽  
J. M. Strunin ◽  
J. M. Layton ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Rat Liver ◽  
Extracellular Ph ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Lactate Metabolism ◽  
Lactate Output ◽  
Lactate Uptake ◽  
The Relationship

1. The relationship between extracellular pH (pHe), intracellular pH (pHi) and lactate uptake was studied in the isolated perfused rat liver during simulated metabolic acidosis. 2. pHi fell to a considerably less extent than pHe when the latter was decreased from pH 7·4 to 6·7. 3. The liver took up lactate when pHi was greater than 7·0; at lower values of pHi lactate output occurred. 4. The relevance of these observations to the control of hepatic pHi and lactate metabolism is discussed.

Neuronal pH Regulation: Constant Normal Intracellular pH is Maintained in Brain during Low Extracellular pH Induced by Acetazolamide—31P NMR Study

1989 ◽  
Vol 9 (3) ◽  
pp. 417-421 ◽  
Author(s):  
Sissel Vorstrup ◽  
Karl Erik Jensen ◽  
Carsten Thomsen ◽  
Ole Henriksen ◽  
Niels A. Lassen ◽  
...  
Keyword(s):  
Intracellular Ph ◽  
Ph Regulation ◽  
Extracellular Ph ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Nmr Study ◽  
Resonance Frequencies ◽  
The Mean ◽  
Ph Decrease ◽  
Body Scanner

The intracellular pH in the brain was studied in six healthy volunteers before and immediately after the administration of 2 g of acetazolamide. Phosphorus-31 nuclear magnetic resonance spectroscopy by a 1.5 tesla whole-body scanner was used. The chemical shift between the inorganic phosphate and the phosphocreatine resonance frequencies was used for indirect assessment of the intracellular pH. The mean baseline intracellular pH was 7.05 ± 0.04 (SD). The mean pH changes obtained at 15-min intervals within the first hour of acetazolamide administration were −0.03 ± 0.04 (SD), −0.02 ± 0.03 (SD), and 0.00 ± 0.04 (SD), i.e., no statistically significant pH decrease was observed during the period where extracellular pH is known to drop markedly. Although several factors contribute to the lack of change of the intraneuronal pH, we will discuss that this observation in addition might suggest a direct intracerebral effect of acetazolamide.

Intracellular bicarbonate of skeletal muscle under different metabolic states

1976 ◽  
Vol 230 (1) ◽  
pp. 228-232 ◽  
Author(s):  
RN Khuri ◽  
SK Agulian ◽  
KK Bogharian
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Equilibrium Potential ◽  
Chronic Metabolic Acidosis ◽  
Cell Ph ◽  
Metabolic States ◽  
Na Depletion ◽  
K Depletion

Intracellular bicarbonate of single muscle fibers in vivo was measured by a direct electrometric method simultaneously with the membrane PD in rats under seven different metabolic states. From the measured intracellular bicarbonate values and the PCO2, the bicarbonate equilibrium potential and the intracellular pH were calculated. The mean intracellular [HCO3-] under normal control conditions was 10.3 +/- 0.7 mM (SE). The intracellular bicarbonate fell significantly in both chronic metabolic acidosis and chronic K+ depletion. In contrast, intracellular bicarbonate was elevated in chronic metabolic alkalosis, K+ loading, and Na+ depletion. Taking intracellular pH as an index of the acid-base status of cells, we find that whereas the calculated cell pH decreased along with the cell bicarbonate in both chronic metabolic acidosis and K+ depletion, cell pH increased along with the bicarbonate only in chronic metabolic alkalosis. Cell pH was unchanged in both chronic K+ loading and Na+ depletion.

Intracellular Buffering in the Dog at Varying CO2 Tensions

1972 ◽  
Vol 42 (3) ◽  
pp. 311-324 ◽  
Author(s):  
J. L. Gamble ◽  
P. J. Zuromskis ◽  
J. A. Bettice ◽  
R. L. Ginsberg
Keyword(s):  
Metabolic Acidosis ◽  
Stroke Volume ◽  
Intracellular Ph ◽  
Concentration Gradient ◽  
Significant Interaction ◽  
Cell Membranes ◽  
Mineral Acid ◽  
Extracellular Ph ◽  
Ion Concentration ◽  
Respiratory Change

1. The effect of varying the Pco2 on the buffering of mineral acid has been investigated. HCl (6 mmol/kg) was infused into anaesthetized-paralysed dogs maintained on a respirator and changes in Pco2 (between 20 and 60 mmHg) were arranged by varying the stroke volume. 2. No significant interaction between buffering of respiratory and metabolic events was discerned. Variations in Pco2 did not alter the efficiency of the buffering of the HCl. The presence or absence of metabolic acidosis did not alter the magnitude of the effect of acute respiratory change on the concentration of extracellular bicarbonate. This response remained between 1·0 and 1·3 mmol/l for changes of 10 mmHg in the Pco2. 3. The buffering of HCl achieved outside the blood and extracellular fluids did not correlate with measured changes in extracellular pH or with predicted changes in intracellular pH. This buffering appears to be associated with changes in the H+ ion concentration gradient across the cell membranes.

Evaluation of whole body nitrogen kinetics in acute metabolic acidosis

1983 ◽  
Vol 37 (2) ◽  
pp. 201-210 ◽  
Author(s):  
M Jeevanandam ◽  
C L Long ◽  
R H Birkhahn ◽  
W S Blakemore
Keyword(s):  
Metabolic Acidosis ◽  
Whole Body ◽  
Acute Metabolic Acidosis

Effect of respiratory acidosis on intracellular pH of the proximal tubule

1986 ◽  
Vol 250 (6) ◽  
pp. F1039-F1045
Author(s):  
B. Trivedi ◽  
R. L. Tannen
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Intracellular Ph ◽  
Chronic Phase ◽  
Respiratory Acidosis ◽  
Glucose Production ◽  
Proximal Tubular ◽  
Acute Metabolic Acidosis ◽  
Urinary Citrate ◽  
Co2 Environment

In contrast to chronic metabolic acidosis, chronic respiratory acidosis does not result in an adaptation in either renal ammonia or glucose production. To examine the possibility that this might be explained by a difference in proximal tubule intracellular pH, the response of two pH-sensitive metabolites, citrate and alpha-ketoglutarate, were assessed. Metabolic acidosis of 3 days duration, induced by drinking 1.5% NH4Cl, significantly reduced urinary citrate excretion (172 to 15 mumol/day) and renal cortical citrate (1.33 to 0.88 mumol/g) and alpha-ketoglutarate (0.90 to 0.46 mumol/g) concentrations in comparison with normal rats. Chronic respiratory acidosis, produced by 3 days in a 10% CO2 environment, lowered systemic pH similar to metabolic acidosis but had no effect on either urinary citrate excretion or renal cortical citrate and alpha-ketoglutarate concentrations. By contrast, acute respiratory acidosis (3, 6, or 24 h duration) reduced urinary citrate excretion and renal cortical citrate and alpha-ketoglutarate concentrations in a fashion similar to acute metabolic acidosis. These data suggest that acute acidosis of either respiratory or metabolic origin lowers the intracellular pH of the proximal tubule. However, when the acid-base abnormality enters the chronic phase, proximal tubular intracellular pH remains low with metabolic acidosis but returns to normal values with respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The Intracellular pH of Human Leucocytes in Response to Acid—Base Changes in Vitro

1976 ◽  
Vol 50 (4) ◽  
pp. 293-299 ◽  
Author(s):  
G. E. Levin ◽  
P. Collinson ◽  
D. N. Baron
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Venous Blood ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Ph Measurements

1. Viable human leucocytes were isolated from venous blood and suspended in artificial media. Intracellular pH measurements were made by the dimethyloxazolidinedione technique in conditions simulating ‘respiratory’ or ‘metabolic’ acid-base disturbances. 2. Normal intracellular pH was 7·11 ± 0·02 (mean ± 2 sd) at an extracellular Pco2 of 5·8 kPa and a bicarbonate concentration of 25 mmol/l. 3. ‘Respiratory’ and ‘metabolic’ acidosis caused little change in pH1 although increases in Pco2 led to relatively greater falls in pH1 than did reduction in external bicarbonate concentration. 4. ‘Respiratory’ and ‘metabolic’ alkalosis caused similar and relatively greater increases in the pH1 when compared with the response to an external acidosis.

Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis

1979 ◽  
Vol 236 (3) ◽  
pp. F240-F245 ◽  
Author(s):  
R. Park ◽  
W. J. Leach ◽  
A. I. Arieff
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Venous Blood ◽  
Respiratory Acidosis ◽  
Normal Liver ◽  
Respiratory Alkalosis ◽  
Arterial Blood ◽  
Acute Metabolic Acidosis

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.

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