Apparent change in the pK'1 of carbonic acid in plasma in response to acute metabolic acidosis in normal subjects

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.

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ACUTE METABOLIC ACIDOSIS: EFFECTS ON ARGININE IN VASOPRESSIN(AVP) RELEASE IN FETAL SHEEP

Pediatric Research ◽

10.1203/00006450-198404001-00264 ◽

1984 ◽

Vol 18 ◽

pp. 137A-137A

Author(s):

Daniel J Faucher ◽

Tom Lowe ◽

About Laptook ◽

John C Porter ◽

Charles R Rosenfeld

Keyword(s):

Metabolic Acidosis ◽

Fetal Sheep ◽

Acute Metabolic Acidosis

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Regulation of AE1 anion exchanger and H + -ATPase in rat cortex by acute metabolic acidosis and alkalosis

Kidney International ◽

10.1038/ki.1997.16 ◽

1997 ◽

Vol 51 (1) ◽

pp. 125-137 ◽

Cited By ~ 95

Author(s):

Ivan Sabolić ◽

Dennis Brown ◽

Stephen L. Gluck ◽

Seth L. Alper

Keyword(s):

Metabolic Acidosis ◽

Anion Exchanger ◽

Rat Cortex ◽

Acute Metabolic Acidosis

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Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

The Scientific World JOURNAL ◽

10.1155/2014/627673 ◽

2014 ◽

Vol 2014 ◽

pp. 1-13 ◽

Cited By ~ 37

Author(s):

María M. Adeva-Andany ◽

Carlos Fernández-Fernández ◽

David Mouriño-Bayolo ◽

Elvira Castro-Quintela ◽

Alberto Domínguez-Montero

Keyword(s):

Chronic Kidney Disease ◽

Metabolic Acidosis ◽

Kidney Disease ◽

Sodium Bicarbonate ◽

Negative Impact ◽

Qtc Interval ◽

Bicarbonate Therapy ◽

Proximal Tubular ◽

Acute Metabolic Acidosis ◽

Renal Proximal Tubular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

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Free Circulating Magnesium and Renal Magnesium Handling during Acute Metabolic Acidosis in Humans

American Journal of Nephrology ◽

10.1159/000013342 ◽

1998 ◽

Vol 18 (3) ◽

pp. 233-236 ◽

Cited By ~ 11

Author(s):

Daniel Blumberg ◽

Alessandro Bonetti ◽

Vincenzo Jacomella ◽

Stellario Capillo ◽

Anita C. Truttmann ◽

...

Keyword(s):

Metabolic Acidosis ◽

Acute Metabolic Acidosis

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Effect of Acute Metabolic Acidosis on Plasma Phosphorus Concentration

Advances in Experimental Medicine and Biology - Phosphate and Minerals in Health and Disease ◽

10.1007/978-1-4615-9167-2_32 ◽

1980 ◽

pp. 263-279

Author(s):

James R. Oster ◽

Guido O. Perez ◽

Albert Castro ◽

Carlos A. Vaamonde

Keyword(s):

Metabolic Acidosis ◽

Phosphorus Concentration ◽

Acute Metabolic Acidosis ◽

Plasma Phosphorus

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Prompt Rise in Urinary Ammonium Excretion Suffices To Mitigate Metabolic Acidosis in an Experimental Animal Model of Severe Normovolemic Hemodilution

Physiological Research ◽

10.33549/physiolres.933491 ◽

2017 ◽

pp. 615-620 ◽

Cited By ~ 1

Author(s):

J. K. TELOH ◽

I. N. WAACK ◽

H. DE GROOT

Keyword(s):

Metabolic Acidosis ◽

Absolute Amount ◽

Ammonium Excretion ◽

Acid Excretion ◽

Urinary Ph ◽

Normovolemic Hemodilution ◽

Proton Excretion ◽

Acute Metabolic Acidosis ◽

Experimental Group ◽

Hasselbalch Equation

Recently, we have established a model of severe stepwise normovolemic hemodilution to a hematocrit of 10 % in rats employing three different colloidal volume replacement solutions (Voluven, Volulyte and Gelafundin) that are routinely used in clinical practice at present. We did not see severe dilutional acidosis as to be expected, but a decline in urinary pH. We here looked on further mechanisms of renal acid excretion during normovolemic hemodilution. Bicarbonate, which had been removed during normovolemic hemodilution, was calculated with the help of the Henderson-Hasselbalch equation. The urinary amount of ammonium as well as phosphate was determined in residual probes. The absolute amount of free protons in urine was obtained from the pH of the respective samples. The amount of protons generated during normovolemic hemodilution was approximately 0.6 mmol. During experimental time (5.5 h), distinct urinary ammonium excretion occurred (Voluven 0.52 mmol, Volulyte 0.39 mmol and Gelafundin 0.77 mmol). Proton excretion via the phosphate buffer constituted 0.04 mmol in every experimental group. Excretion of free protons was in the range of 10-6 mmol. The present data prove that the prompt rise in urinary ammonium excretion is also valid for acute metabolic acidosis originating from severe normovolemic hemodilution.

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Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

Journal of Applied Physiology ◽

10.1152/jappl.1965.20.3.443 ◽

1965 ◽

Vol 20 (3) ◽

pp. 443-452 ◽

Cited By ~ 104

Author(s):

R. A. Mitchell ◽

C. T. Carman ◽

J. W. Severinghaus ◽

B. W. Richardson ◽

M. M. Singer ◽

...

Keyword(s):

Metabolic Acidosis ◽

Active Transport ◽

Respiratory Acidosis ◽

Normal Subjects ◽

Respiratory Alkalosis ◽

Regulation Of Respiration ◽

Respiratory Drive ◽

Acid Base ◽

Peripheral Chemoreceptors ◽

Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

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Effect of temperature on arterial blood gas tensions and pH during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1964.19.2.243 ◽

1964 ◽

Vol 19 (2) ◽

pp. 243-245 ◽

Cited By ~ 23

Author(s):

Alf Holmgren ◽

Malcolm B. McIlroy

Keyword(s):

Metabolic Acidosis ◽

Normal Subjects ◽

Bicycle Ergometer ◽

Effect Of Temperature ◽

Membrane Diffusion ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Capillary Membrane ◽

Severe Exercise ◽

Alveolar Capillary

We measured arterial blood Po2, Pco2 and pH at rest and during a standard exercise test on a bicycle ergometer in ten normal subjects. In five we measured esophageal and five arterial blood temperature during the exercise and corrected the arterial blood values to the temperature at the time the samples were collected. We found an average rise in temperature of 1 C (range 0.2–1.6 C) during exercise lasting about 30 min at loads up to an average of 1,200 kg-m/min. At the highest load the average correction for PaOO2 was 5.6 mm Hg, for PaCOCO2 1.6 mm Hg and for pH 0.014 units. Our corrected values showed a fall in PaCOCO2 and pH and a rise in PaOO2 during severe exercise. These findings are compatible with the development of a metabolic acidosis during severe exercise and indicate that our subjects were not limited by diffusion across the alveolar-capillary membrane. metabolic acidosis; alveolar capillary membrane diffusion; hyperventilation; PaOO2 and PaCOCO2 in severe exercise Submitted on June 17, 1963

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