Dependence of the apparent bicarbonate space on initial plasma bicarbonate concentration and carbon dioxide tension in neonatal calves with diarrhea, acidemia, and metabolic acidosis

These experiments were performed to examine the buffering functions of skeletal carbon dioxide during metabolic acidosis. Acidosis of several days duration was produced in rats either by inclusion of acidogenic substances in the diet or by chemical induction of diabetic ketoacidosis. Titrimetric methods were used to measure the carbon dioxide content of bone, which was divided into readily exchangeable and slowly exchangeable pools according to a model described in the text. Acid feeding resulted in a mild acidemia (blood pH greater than 7.25), whereas profound metabolic acidemia occurred during diabetic ketoacidosis (blood pH less than 7.00). Total bone carbon dioxide was reduced during both forms of metabolic acidosis. This reduction in skeletal carbon dioxide occurred within the first 24 h after the onset of metabolic acidosis, was associated with a decline in the readily exchangeable fraction of skeletal carbon dioxide, and was directly proportional to the declines in extracellular bicarbonate concentration and plasma carbon dioxide tension.

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Role of endothelin-1 in renal regulation of acid-base equilibrium in acidotic humans

AJP Renal Physiology ◽

10.1152/ajprenal.00309.2012 ◽

2012 ◽

Vol 303 (7) ◽

pp. F991-F999 ◽

Cited By ~ 7

Author(s):

Alexandra Pallini ◽

Henry N. Hulter ◽

Jurgen Muser ◽

Reto Krapf

Keyword(s):

Metabolic Acidosis ◽

Bicarbonate Concentration ◽

Acid Base ◽

Endothelin 1 ◽

Plasma Bicarbonate ◽

Human Volunteers ◽

Acid Base Equilibrium ◽

Normal Human ◽

Mineralocorticoid Activity

Endothelin-1 inhibits collecting duct sodium reabsorption and stimulates proximal and distal tubule acidification in experimental animals both directly and indirectly via increased mineralocorticoid activity. Diet-induced acid loads have been shown to increase renal endothelin-1 activity, and it is hypothesized that increased dietary acid-induced endothelin-1 activity may be a causative progression factor in human renal insufficiency and that this might be reversed by provision of dietary alkali. We sought to clarify, in normal human volunteers, the role of endothelin-1 in renal acidification and to determine whether the effect is dependent on dietary sodium chloride. Acid-base equilibrium was studied in seven normal human volunteers with experimentally induced metabolic acidosis [NH4Cl 2.1 mmol·kg body weight (BW)−1·day−1] with and without inhibition of endogenous endothelin-1 activity by the endothelin A/B-receptor antagonist bosentan (125 BID p.o./day) both during dietary NaCl restriction (20 mmol/day) and NaCl repletion (2 mmol NaCl·kg BW−1·day−1). During NaCl restriction, but not in the NaCl replete state, bosentan significantly increased renal net acid excretion in association with stimulation of ammoniagenesis resulting in a significantly increased plasma bicarbonate concentration (19.0 ± 0.8 to 20.1 ± 0.9 mmol/l) despite a decrease in mineralocorticoid activity and an increase in endogenous acid production. In pre-existing human metabolic acidosis, endothelin-1 activity worsens acidosis by decreasing the set-point for renal regulation of plasma bicarbonate concentration, but only when dietary NaCl provision is restricted.

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Ventilatory response to chronic metabolic acidosis and alkalosis in the dog

Journal of Applied Physiology ◽

10.1152/jappl.1984.56.6.1640 ◽

1984 ◽

Vol 56 (6) ◽

pp. 1640-1646 ◽

Cited By ~ 22

Author(s):

N. E. Madias ◽

W. H. Bossert ◽

H. J. Adrogue

Keyword(s):

Metabolic Acidosis ◽

Metabolic Alkalosis ◽

Ventilatory Response ◽

Wide Spectrum ◽

Bicarbonate Concentration ◽

Acid Base ◽

Arterial Pco2 ◽

Plasma Bicarbonate ◽

Oral Sodium ◽

Chronic Change

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

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The Ventilatory Response in Diabetic Ketoacidosis

Clinical Science ◽

10.1042/cs0460539 ◽

1974 ◽

Vol 46 (4) ◽

pp. 539-549 ◽

Cited By ~ 1

Author(s):

M. Fulop ◽

N. Dreyer ◽

H. Tannenbaum

Keyword(s):

Metabolic Acidosis ◽

Diabetic Ketoacidosis ◽

Ventilatory Response ◽

Hydrogen Ion ◽

Inverse Relation ◽

Bicarbonate Concentration ◽

Plasma Bicarbonate ◽

Arterial Blood ◽

Blood Ph ◽

Ion Activity

1. Previous studies of the ventilatory response to metabolic acidosis have usually considered only patients with arterial blood pH above 7·10. To define the response during more severe acidaemia, arterial CO2 tension and pH were measured in fifty-three episodes of diabetic ketoacidosis, including twenty-four with pH below 7·10, and ten with pH below 7·00. 2. The relation between arterial CO2 tension, and both blood pH and plasma bicarbonate concentration, in these cases with generally severe metabolic acidaemia (mean pH 7·12 ± SD 0·13), was very similar to the relations between those variables found by others in patients with less severe acidaemia, such as that due to renal failure. 3. As arterial blood hydrogen ion activity increased, arterial CO2 tension decreased inversely, reflecting well-sustained hyperventilation, even during profound acidaemia. 4. The inverse relation between arterial CO2 tension and hydrogen ion activity suggests that during metabolic acidosis, alveolar ventilation increases in direct proportion to the increased blood hydrogen ion activity.

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CERTAIN ASPECTS OF THE RENAL REGULATION OF BODY COMPOSITION

PEDIATRICS ◽

10.1542/peds.14.6.567 ◽

1954 ◽

Vol 14 (6) ◽

pp. 567-572

Author(s):

ROBERT E. COOKE

Keyword(s):

Carbon Dioxide ◽

Extracellular Space ◽

Carbonic Acid ◽

Plasma Concentrations ◽

Extracellular Volume ◽

Extracellular Fluid ◽

Carbon Dioxide Tension ◽

Plasma Sodium ◽

Renal Tubules ◽

Bicarbonate Concentration

THE pH of extracellular fluid is determined by the ratio of the plasma concentrations of bicarbonate ion to carbonic acid, as given in the classical Henderson-Hasselbach equation. [See Equation in Source Pdf] The denominator the carbonic acid concentration, [H2CO3], is proportional to the carbon dioxide tension of the blood. The carbon dioxide tension (pCO2) is primarily dependent upon respiratory function, since metabolism (hence carbon dioxide production) is relatively constant. The numerator of the equation—the bicarbonate concentration of extracellular fluid—is determined by the difference between nonvolatile cations and anions. Since there are almost limitless quantities of bicarbonate available to the organism from cell metabolism, [See Equation in Source Pdf] bicarbonate concentration must change whenever nonvolatile cation (largely sodium) is altered in relation to nonvolatile anion (largely chloride). Thus in most states extracellular bicarbonate concentration is dependent upon the ratio of sodium to chloride in extracellular fluid. The quantity of water filtered at the glomeruli and reabsorbed by the renal tubules each day is approximately 15 times the extracellular volume. The quantity of sodium chloride filtered and reabsorbed daily is approximately 15 times that contained in the extracellular space and 150 times that usually ingested and excreted each day. Therefore, the ratio of plasma sodium to chloride in any steady state is determined by the composition of the renal tubular reabsorbate, as Cushny pointed over 30 years ago. In a sense the kidney perfuses the extracellular space with large quantities of tubular reabsorbate. Tubular reasorbate—the net quantity of materials reabsorbed by the tubules. This term is analogous to glomerular filtrate—the quantity of materials filtered by the glomeruli.

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PRE- AND POSTBRANCHIAL CARBON DIOXIDE CONTENT OF RAINBOW TROUT (ONCORHYNCHUS MYKISS) BLOOD AFTER CATECHOLAMINE INJECTION

Journal of Experimental Biology ◽

10.1242/jeb.180.1.315 ◽

1993 ◽

Vol 180 (1) ◽

pp. 315-322

Author(s):

M. Nikinmaa ◽

L. Vihersaari

Keyword(s):

Carbon Dioxide ◽

Rainbow Trout ◽

Unit Volume ◽

Carbon Dioxide Production ◽

Carbon Dioxide Tension ◽

Co2 Removal ◽

Plasma Bicarbonate ◽

Rainbow Trout Oncorhynchus Mykiss ◽

Secondary Lamellae ◽

Co2 Excretion

It is generally accepted that plasma bicarbonate is the major source of carbon dioxide excreted in the gills of teleost fish (Perry, 1986). Although anion exchange across the membrane of rainbow trout erythrocytes is rapid, with a half-time of 0.8 s for chloride equilibration at 15 °C (Romano and Passow, 1984), the rate of bicarbonate influx into the erythrocytes limits the rate of conversion of plasma bicarbonate to carbon dioxide and, thereby, carbon dioxide excretion per unit volume of blood in gills, because the residence time of blood in the secondary lamellae of the gills is only 1–6 s (Hughes et al. 1981; Bhargava et al. 1992). Thus, factors that reduce the net rate of bicarbonate influx through the anion exchanger may reduce the efficiency of carbon dioxide excretion in gills. The effect is, however, temporary. If carbon dioxide production remains constant, the reduction of carbon dioxide excretion will increase the venous carbon dioxide tension and content, thus increasing the diffusion gradient across the gills and speeding up CO2 removal until the CO2 excretion again matches production.

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Effect of growth hormone on renal and systemic acid-base homeostasis in humans

AJP Renal Physiology ◽

10.1152/ajprenal.1998.274.4.f650 ◽

1998 ◽

Vol 274 (4) ◽

pp. F650-F657 ◽

Cited By ~ 4

Author(s):

Anita Sicuro ◽

Katia Mahlbacher ◽

Henry N. Hulter ◽

Reto Krapf

Keyword(s):

Growth Hormone ◽

Metabolic Acidosis ◽

Recombinant Human Growth Hormone ◽

Human Growth ◽

Normal Subjects ◽

Acid Excretion ◽

Bicarbonate Concentration ◽

Acid Base ◽

Plasma Bicarbonate ◽

Net Acid Excretion

The effects of recombinant human growth hormone (GH, 0.1 U ⋅ kg body wt−1 ⋅ 12 h−1) on systemic and renal acid-base homeostasis were investigated in six normal subjects with preexisting sustained chronic metabolic acidosis, induced by NH4Cl administration (4.2 mmol ⋅ kg body wt−1 ⋅ day−1). GH administration increased and maintained plasma bicarbonate concentration from 14.1 ± 1.4 to 18.6 ± 1.1 mmol/l ( P < 0.001). The GH-induced increase in plasma bicarbonate concentration was the consequence of a significant increase in net acid excretion that was accounted for largely by an increase in renal [Formula: see text]excretion sufficient in magnitude to override a decrease in urinary titratable acid excretion. During GH administration, urinary pH increased and correlated directly and significantly with urinary[Formula: see text] concentration. Urinary net acid excretion rates were not different during the steady-state periods of acidosis and acidosis with GH administration. Glucocorticoid and mineralocorticoid activities increased significantly in response to acidosis and were suppressed (glucocorticoid) or decreased to control levels (mineralocorticoid) by GH. The partial correction of metabolic acidosis occurred despite GH-induced renal sodium retention (180 mmol; gain in weight of 1.8 ± 0.2 kg, P< 0.005) and decreased glucocorticoid and mineralocorticoid activities. Thus GH (and/or insulin-like growth factor I) increased plasma bicarbonate concentration and partially corrected metabolic acidosis. This effect was generated in large part by and maintained fully by a renal mechanism (i.e., increased renal NH3 production and[Formula: see text]/net acid excretion).

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