Changes In Bicarbonate Concentration Research Articles

Effects of climate and acidic deposition on interannual variations of stream water chemistry in forested watersheds in the Shimanto River Basin, southern Japan

AbstractAlthough the amount of acidic deposition has recently decreased in Japan, it has still deteriorated some forest ecosystems during the past several decades. Moreover, recent climate changes can affect stream water chemistry. We investigated the temporal trend and effects of climate conditions on stream water chemistry for more than 20 years in two areas (Yusuhara and Taisho) in the Shmanto River Basin, southern Japan, where the effects of acidic deposition are considered to be modest. Stream water samples were collected monthly from three forest watersheds selected at each site. The annual means of the stream chemistry were predicted by multiple regression analysis. The ammonium, nitrate, and sulfate concentrations in the bulk precipitation have decreased at Yusuhara, and the sodium, magnesium, calcium, chloride, nitrate, and sulfate concentrations in the stream water have decreased in both areas. The nitrate and sulfate concentrations apparently responded to the decreasing input of acidic deposition. The sunlight hours were positively related with the potassium, magnesium, calcium, nitrate, sulfate, and bicarbonate concentrations in stream water. The results suggest that long sunlight hours boost the photosynthetic activities, thus promoting soil respiration and decomposition of soil organic matter. Moreover, a higher carbonic acid concentration in the soil solution promotes cation weathering and carbonic acid dissociation to bicarbonate. Given the decreasing trends in magnesium and calcium concentration with no change in bicarbonate concentration, we inferred that previousinputs of acidic deposition enhanced the rate of rock weathering.

Using europium(III) complex of 1,4,7,10-tetraazacyclododecane-1,4,7-triacedic acid Eu.DO3A as a luminescent sensor for bicarbonate

Sensing of analytes in biological fluids and biotechnological production media remains a challenge. Here, the luminescent response of the europium (III) complex of 1,4,7,10-tetraazacyclododecane-1,4,7-triacetic acid (DO3A) to bicarbonate was investigated in detail. The response of Eu.DO3A to changes in bicarbonate concentration was studied in different buffers, and the influence of ionic strength, pH, and specific ions was determined. The response is found to depend on pH and ionic strength, but it is not possible to separate contributions from the sensing event from those in the bicarbonate activity. Prior to demonstrating the ability to determine the bicarbonate concentration in bioproduction media and serum, the influence of competing carboxy anions was evaluated. It is established that while competing anions bind stronger to the responsive complex, at the relevant concentration their contribution to the recorded signal is negligible. We are thus able to conclude that Eu.DO3A is a good platform for building a bicarbonate sensor.

Protocolo diagnóstico de la acidosis metabólica

Metabolic acidosis is an acid-base disorder tends to produce acidemia (decrease in pH) for the primary changes in bicarbonate concentration. It is classified into normochloremic or hyperchloremic by the value of anion gap (AG) of the plasma; parameter representing the difference between the main positive charge (cations) and negative (anions). The cause of metabolic acidosis should be assessed by history and clinical context, but any assessment of acidosis should include blood gas, electrolyte determination, measuring response and compensatory respiratory, AG and ΔAG/ΔHCO▪.

Acute regulation of hematocrit and acid–base balance in chicken embryos in response to severe intrinsic hypercapnic hypoxia

The regulation of blood acid–base balance and hematology in day 15 chicken embryos in response to partial water submersion (with egg's air cell in air) and complete submersion producing severe intrinsic hypercapnic hypoxia and recovery in air was studied. The acid–base disturbance during submersion was characterized by initial rapid respiratory changes and then superseded by metabolic processes, resulting in a large progressive hysteresis. Throughout submersion and recovery, blood lactate concentration changed swiftly along with the changes in bicarbonate concentration ([HCO3−]), indicating that anaerobic glycolysis determined overall acid–base disturbances. Both partial and complete submersion produced large, rapid increases in hematocrit through proportional increases in mean corpuscular volume and red blood cell concentration. Death ensued once the internal pool of O2 was exhausted and/or the acid–base disturbance became too severe for survival (i.e., [HCO3−]a<∼10mmolL−1). However, embryos recovered from acid–base and hematological disturbances within 120min recovery in air after short bouts of complete (20min) or partial (60min) submersion, suggesting that shorter severe intrinsic hypercapnic hypoxia does not compromise viability of embryos.

Evidence for the optical signalling of changes in bicarbonate concentration within the mitochondrial region of living cells

Image and spectral intensity from bicarbonate-selective europium(III) probes localised in the mitochondria of cells is modulated reversibly by variation of external pCO(2), and is suppressed by addition of the carbonic anhydrase inhibitor, acetazolomide.

The acid–base effects of free water removal from and addition to oxygenated and deoxygenated whole blood: an in vitro model of contraction alkalosis and dilutional acidosis

This study was conducted to describe the acid-base effects of hydration and dehydration of oxygenated and deoxygenated whole blood. Whole blood samples from goats were equilibrated in a tonometer to a partial pressure of carbon dioxide of 40 mm Hg and oxygen (PO₂) of 100 mm Hg or 30 mm Hg. Contraction alkalosis was achieved by evaporating blood samples to 80% of the original volume. Dilutional acidosis was achieved by increasing the blood sample volume by 20% by addition of sterile water. Acid-base, electrolyte, hemoglobin, lactate, albumin, and phosphorus concentrations were measured at baseline and after dehydration or hydration. A 20% dehydration of whole blood caused a 22% increase in sodium concentration and a significant increase in base excess of +3 mEq/L (P < 0.01); bicarbonate concentration increased only 7% to 9%. A concurrent increase was found in phosphorus, albumin, hemoglobin, and lactate concentrations. A 20% dilution of whole blood caused a 21% decrease in sodium concentration and a significant decrease in base excess of -5 mEq/L (P < 0.01) with an 11% to 15% decrease in bicarbonate concentration. A concurrent decrease was found in phosphorus, albumin, and hemoglobin concentrations. No significant difference was observed between the acid-base effects on oxygenated versus deoxygenated blood in any experiment. Dilutional acidosis and contraction alkalosis of whole blood are complex acid-base disorders resulting from direct changes in bicarbonate concentration in combination with changes in the concentration of weak plasma acids and buffering reactions. Therefore, bicarbonate concentration does not change to the same degree as the magnitude of contraction or dilution.

Acid-base and blood gas analysis

Abstract The concentration of hydrogen ions is one of the most tightly controlled systems in the body. Defence of normal pH is thought to be from three basic mechanisms: respiratory control of carbon dioxide, renal excretion of acids, and plasma buffering systems. The traditional approach to acid–base control centres on the Henderson–Hasselbalch equation, in which pH can be defined as the ratio of bicarbonate to carbon dioxide. Alterations in pH result from changes in carbon dioxide (respiratory) or bicarbonate (metabolic). Most pH disturbances can be classified into one of four main types: respiratory acidosis; respiratory alkalosis; metabolic acidosis; metabolic alkalosis. The Stewart hypothesis is an alternative approach to acid–base analysis. It challenges the concept that changes in bicarbonate concentration can alter pH. This theory, based on mathematical solution, is that only three things, alone or in combination, can determine the hydrogen ion concentration: strong ion difference (net charge balance of dissociated ions in plasma); partial pressure of carbon dioxide; and the sum of acids present.

Determination of kinetic parameters and simulation of early CO 2 production from the Boom Clay kerogen under low thermal stress

The main purpose of the present study is to evaluate the nature and amount of gaseous compounds that would be generated from the Boom Clay kerogen due to the foreseen thermal stress associated with the geological disposal of high activity nuclear waste. To this end, pyrolysis experiments were carried out on this low maturity, O-rich kerogen with focus on mild conditions, including Rock–Eval and closed pyrolyses using a wide range of temperature/time conditions. The residual kerogen recovered after the closed pyrolyses was re-examined by Rock–Eval and elemental analyses and the components of the gas fractions were identified and quantified by gas chromatography. These experiments showed substantial production of CO 2 (corresponding to ca. 1/5 of the total O content of the kerogen) under mild thermal stress. The kinetic parameters (frequency factor and distribution of activation energy) of this early production of CO 2 were determined and used to simulate the possible consequences for the deep disposal of highly radioactive waste. Extrapolation to thermal stresses, corresponding to 80 and 100 °C over 1 ka, indicated that this production of CO 2 might influence the geochemistry and perhaps therefore the effectiveness of the geological barrier. For example, unless diffusion out of the heated zone counterbalances the effect of CO 2 generation, significant acidification and large changes in bicarbonate concentration may take place, in the interstitial water of the clay, at a time scale of only tens to a few hundred years.

Acid-base and blood gas analysis

The concentration of hydrogen ions is one of the most tightly controlled systems in the body. Defence of normal body pH is thought to be from three basic mechanisms: respiratory control of carbon dioxide, renal excretion of acids, and plasma buffering systems. The traditional approach to acid-base control centres around the Henderson-Hasselbalch equation, in which pH can be defined as the ratio of bicarbonate to carbon dioxide. Alterations in pH result from changes in carbon dioxide (respiratory) or bicarbonate (metabolic). Most pH disturbances can be classified into one of four main types. 1 Respiratory acidosis, where the primary change is an increase in carbon dioxide with attempted compensatory increase in bicarbonate (e.g. ventilatory failure). 2 Respiratory alkalosis, where the primary change is a fall in carbon dioxide followed by attempted compensatory fall in bicarbonate (e.g. hyperventilation). 3 Metabolic acidosis, where there is a fall in bicarbonate with attempted compensatory fall in carbon dioxide (e.g. aspirin overdose). 4 Metabolic alkalosis, where the primary change is raised bicarbonate with attempted compensatory increase in carbon dioxide (e.g. gastric acid losses). The Stewart hypothesis is an alternative approach to acid-base analysis. It challenges the concept that changes in bicarbonate concentration can alter pH. This theory, based on mathematical solution, is that only three things, alone or in combination, can determine the hydrogen ion concentration: strong ion difference (net charge balance of dissociated ions in plasma); partial pressure of carbon dioxide; and the sum of acids present.

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition.

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate concentration) in blood plasma. The difference between -delta[La].delta pH-1 and delta[HCO3-].delta pH-1 yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, delta[HCO3-].delta pH-1 can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7-8 days (group 1) or 11-12 days (group 2) after their return from a Himalayan expedition (2800-7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia -delta[La].delta pH-1 amounted to [mean (SEM)] 92 (6) mmol.l-1 before altitude, of which 19 (4), 48 (1) and 25 (3) mmol.l-1 were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude -delta[La].delta pH-1 was increased to 128 (12) mmol.l-1 (P < 0.01) in group 1 and decreased to 72 (5) mmol.l-1 in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol.l-1 in group 1 and to 10 (2) mmol.l-1 in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol.l-1]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La- and H+ across cell membranes is differently influenced by high-altitude acclimatization.

Effect of pH on citrate reabsorption in the proximal convoluted tubule.

Urinary citrate is an important endogenous inhibitor of calcium nephrolithiasis. Systemic acidosis increases renal citrate reabsorption (decreases urinary excretion) and hence is associated with nephrolithiasis; systemic alkali administration increases citrate excretion. We studied the mechanism by which acidosis and alkalosis alter citrate reabsorption in the proximal convoluted tubule, the predominant nephron segment reabsorbing citrate. Tubules were perfused in vitro and citrate reabsorption was measured by use of luminal [14C]citrate. Changes in solution pH were accomplished by changes in bicarbonate concentration with constant PCO2. Decreasing peritubular pH acutely from 7.4 to 7.2 caused an increase in citrate reabsorption. However, the change seen with an acid peritubular pH was abolished by additional buffering of the luminal solution. Increasing peritubular pH from 7.4 to 7.6 resulted in a fall in citrate reabsorption that was not significantly greater than a time-dependent fall in citrate reabsorption in this preparation. The effect of luminal pH on proximal citrate reabsorption was also examined directly. Decreasing perfusate (luminal) pH from 7.4 to 7.2 with constant peritubular pH increased citrate reabsorption. Increasing perfusate pH to 7.6 decreased citrate reabsorption insignificantly (0.1 less than P less than 0.2). These data suggest that luminal pH in the proximal tubule is an important determinant of alterations in citrate reabsorption with acid-base disorders. The effect of luminal pH on citrate reabsorption is probably due to a change in concentration of the transported ionic species, citrate2-.

The effect of prolonged pancreatic secretion on blood acid-base balance in the conscious dog.

Prolonged near maximal pancreatic secretion in conscious dogs has been found to result in a metabolic acidosis. This is mild and is accompanied by respiratory and other forms of compensation. Measurements of blood bicarbonate or base-excess changes cannot be used to estimate pancreatic bicarbonate output. The acidosis caused by pancreatic secretion cannot explain the changes in bicarbonate concentration seen in pancreatic juice during prolonged secretion.

The influence of graded degrees of chronic hypercapnia on the acute carbon dioxide titration curve.

Studies were carried out to determine the influence of the chronic level of arterial carbon dioxide tension upon the buffering response to acute changes in arterial carbon dioxide tension. After chronic adaptation to six levels of arterial CO(2) tension, ranging between 35 and 110 mm Hg, unanesthetized dogs underwent acute whole body CO(2) titrations. In each instance a linear relationship was observed between the plasma hydrogen ion concentration and the arterial carbon dioxide tension. Because of this linear relationship, it has been convenient to compare the acute buffering responses among dogs in terms of the slope, dH(+)/dPaco(2). With increasing chronic hypercapnia there was a decrease in this slope, i.e. an improvement in buffer capacity, which is expressed by the equation dH(+)/dPaco(2)=-0.005 (Paco(2))(chronic) + 0.95. In effect, the ability to defend pH during acute titration virtually doubled as chronic Paco(2) increased from 35 to 110 mm Hg. The change in slope, dH(+)/dPaco(2), was the consequence of the following two factors: the rise in plasma bicarbonate concentration which occurs with chronic hypercapnia of increasing severity, and the greater change in bicarbonate concentration which occurred during the acute CO(2) titration in the animals with more severe chronic hypercapnia. These findings demonstrate the importance of the acid-base status before acute titration in determining the character of the carbon dioxide titration curve. They also suggest that a quantitative definition of the interplay between acute and chronic hypercapnia in man should assist in the rational analysis of acid-base disorders in chronic pulmonary insufficiency.

Mechanisms of placental carbon dioxide transfer

Following acetazolamide infusions into four fetal monkeys (73 to 98 mg per kg) consistent increases in Pco 2 and decreases in pH were measured in umbilical artery blood. These changes were not accompanied by significant changes in bicarbonate concentration and in only one experiment by an increase in lactate content.

Bicarbonate and chloride of rat brain during infusion-induced changes in bicarbonate concentration of blood.

The bicarbonate concentrations at differentP CO 2 levels (bicarbonate-CO2 dissociation curve) and the chloride concentrations of brain and blood were studied in rats with respiratory or non-respiratory modifications of the acid-base balance. The CO2 dissociation curves were obtained in vivo by imposing on anaesthetized and curarized animals of identical experimental groups differentP CO 2 levels during 20 min either by maintaining a normal ventilation volume with air, by increasing the ventilation volume 2.5–3 times or by giving 10% CO2 in air. At the end of the exposure period arterial blood was collected and the brain was frozen in liquid nitrogen. When groups of rats were kept during 6 hours in 12% CO2 in air, the CO2 dissociation curves of blood and brain were displaced to higher HCO 3 − values, compared to the curves obtained after an identical period of hypocapnia realized by giving a hypoxic gas mixture (10% O2 in nitrogen). Chloride concentrations showed shifts in the other direction. In other groups of rats shifts of the CO2 dissociation curve in plasma were rapidly produced by intravenous infusion of acid (HCl 150 mM/l) or alkaline (NaHCO3 150 mM/l) solutions during 20 min, 6 hours or 24 hours. Despite the marked modification in plasma, the CO2 dissociation curve of brain was not displaced after 6 hours and showed only a very small shift after 24 hours. Chloride concentration in brain showed changes in the same direction as in blood plasma after 6 hours.

Brain CO2 buffering capacity in respiratory acidosis and alkalosis.

ArticleBrain CO2 buffering capacity in respiratory acidosis and alkalosis.H Kazemi, D C Shannon, and E Carvallo-GilH Kazemi, D C Shannon, and E Carvallo-GilPublished Online:01 Feb 1967https://doi.org/10.1152/jappl.1967.22.2.241MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByTransport of ions across the choroid plexus epitheliumAcid–base balance and cerebrovascular regulation26 November 2021 | The Journal of Physiology, Vol. 599, No. 24Acid/Base Transporters in CSF Secretion and pH Regulation18 April 2020The choroid plexus sodium-bicarbonate cotransporter NBCe2 regulates mouse cerebrospinal fluid pH12 August 2018 | The Journal of Physiology, Vol. 596, No. 19The murine choroid plexus epithelium expresses the 2Cl−/H+ exchanger ClC-7 and Na+/H+ exchanger NHE6 in the luminal membrane domainHelle H. 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Buffering systems in the mouth

1. 1. The buffering systems in saliva, salivary sediment, and plaque are discussed. Bicarbonate is the major buffer in activated saliva, phosphate accounting for the remainder of the buffering effect. Salivary mucoid and bacteria have an insignificant buffer action in whole saliva. In resting saliva, the buffering effect is decreased because of the smaller concentration of bicarbonate in resting saliva than in activated saliva; therefore, phosphate becomes relatively more important. Salivary sediment and plaue have different buffering systems. The former has a variable amount of adsorbed bicarbonate which plaque does not possess. 2. 2. The effect of eating a meal on the buffering power of the saliva of fifteen subjects was examined. A constant increase or decrease in buffering after the meal was not observed. 3. 3. Paraffin-activated saliva, collected during a period similar to that taken for the meal, did not show any appreciable changes in buffering properties, as determined by comparison of the first and last five-minute samples of saliva. During the test period, however, changes were observed which were paralleled by changes in bicarbonate concentration. No consistent relation was found between HCO ′ 3, Na +, and K + concetrations and volume of sample. 4. 4. A significant relation was observed between buffering effect for the sample, pH 7.0 to 6.0, and the volume of five-minute samples of activated saliva for a group of sixty-seven subjects. 5. 5. The limitations of the buffering test in attempting to assess caries susceptibility were investigated in a group of sixty-five subjects.