Weak Acid Buffer Research Articles

Simultaneous determination of dihydroxybenzene and phenylenediamine positional isomers using capillary zone electrophoresis coupled with amperometric detection

In general capillary zone electrophoresis (CZE) separation models, o-, m-, and p-phenylenediamine isomers can be separated in a weak acidic running buffer for their pK(a) values being 4.52, 5.64, 6.04, respectively, while o-, m-, and p-dihydroxybenzene isomers can be separated in a weak basic buffer for their pK(a) values being 9.40, 9.40 and 10.04, respectively. So, it is hard to find a suitable running buffer at a fixed pH in normal CZE for simultaneous separation of these two groups of positional isomers. In this paper, a novel method based on alternately running two different pH buffers in CZE coupled with amperometric detection (CZE-AD) was designed to simultaneously determine these two groups of positional isomers. It is found that when two different pH running buffers were employed alternately under appropriate order and time, the six analytes could be separated perfectly in less than 20 min and the detection limits were as low as 10(-7) mol/L. Furthermore, the effects of working electrode potential, pH and concentration of running buffer, separation voltage and injection time on CZE-AD were investigated. Experimental results demonstrated that the introduced method was practical to simultaneously determine two groups of positional isomers with different pK(a) and had some advantages of high sensitivity, good repeatability and small sample requirement.

Resonance Rayleigh scattering method for the determination of chitosan with some anionic surfactants

In weak acidic buffer medium, chitosan binding with an anionic surfactant, such as sodium dodecyl benzene sulphonate (SDBS), sodium lauryl sulphate (SLS) or sodium dodecyl sulphonate (SDS), can result in a significant enhancement of resonance Rayleigh scattering (RRS) intensity. The results showed that under optimum conditions the enhanced RRS intensity is proportional to the concentration of chitosan in the range 0.10-20.0 microg/mL for SDBS, 0.27-15.0 microg/mL for SLS and 0.20-15.0 microg/mL for SDS. Among these, the sensitivity of SDBS is the highest and its detection limit for chitosan is 29 ng/mL, while those of SLS and SDS are 83 and 61 ng/mL, respectively. The method has good selectivity and was applied to the determination of trace amounts of chitosan in practical samples with satisfactory results. Therefore, a simple and convenient method with high sensitivity and selectivity for the determination of chitosan was established.

In Situ Measurements of pH Changes in β-Lactoglobulin Solutions under High Hydrostatic Pressure

A novel in situ method, in which the spectral changes of aqueous solutions under pressure are measured using optical pH indicators in a high-pressure spectrophotometer, has been developed in order to provide a quantitative description of the pressure dependence of acid/base equilibria of proteins. The self-consistent method, insensitive to compressibility, was developed for measurement of changes in pH with pressure based on alpha-naphthyl red and neutral red as these indicators were found to have pressure insensitive pKa values. The method was validated for up to 500 MPa by measurement of the pressure-dependence of the weak acid buffers acetic acid/acetate and imidazolium/imidazole from which volumes of dissociation of DeltaV degrees = -11.2 and 3.7 mL/mol, respectively, were established. Succinic acid/hydrogensuccinate was surprisingly insensitive to pressure with DeltaV degrees = -0.9 mL/mol. For beta-lactoglobulin B in an unbuffered aqueous solution with ionic strength of 0.05 M and pH 4, pressure up to 300 MPa increased pH up to 1.5 units depending on concentration (up to 5 mg/mL investigated), followed by a decrease to the initial pH 4 for pressure up to 500 MPa. The surprising increase in pH at pressure up to 300 MPa is suggested to be caused by an increase in the effective pKa values of aspartic acid and glutamic acid side chain in hydrophobic compartments of the protein created by pressure denaturation, leading to a binding of water protons and an increase in free hydroxide ions. For higher pressure the carboxylic side chains in the fully denatured protein again becomes exposed to the solvent, and pH decreases to the initial pH of the aqueous system.

A Highly Sensitive Resonance Rayleigh Scattering Method for the Determination of Vitamin B1 with Gold Nanoparticles Probe

In weakly acidic buffer medium, vitamin B1 (VB1) interacts with gold nanoparticles to form a binding product, which resulted in a significant enhancement of resonance Rayleigh scattering (RRS) intensity and the appearance of a new RRS spectrum. The maximum RRS peak was at 368 nm, and there are three smaller scattering peaks that were at 284 nm, 440 nm and 495 nm, respectively. The enhanced RRS intensity (ΔI) was directly proportional to the concentration of VB1 in the range of 0–2.8 × 10−7 mol L−1. The method had high sensitivity and its detection limit (3σ) was 0.9 ng mL−1. The optimum conditions and the influencing factors have been investigated. The method had good selectivity, which could be observed from the influence of coexisting substances. A sensitive, simple and fast RRS method for the determination of VB1 with gold nanoparticle probe has been developed. In addition, the reasons for RRS enhancement were discussed.

Corrosion Behavior of Polymer-Bonded NdFeB-Based Nanocrystalline Magnets

The corrosion resistance of polymer bonded nanocrystalline NdFeB magnets with Nd-rich, stoichiometric, and Fe-rich compositions and that of their main constituent single phases is assessed in aqueous environments. For the evaluation of corrosion properties, gravimetric tests as well as potentiodynamic polarization measurements were performed in different nitrogen-purged electrolytes: 0.1 M sulfuric acid (pH=1), 0.5 M phthalate buffer (pH=5), and 0.1 M sodium hydroxide (pH=13). The single phases show anodic dissolution in strong acidic environment and stable passivation in alkaline solution. In weakly acidic phthalate buffer Nd-rich and Fe phases exhibit limited passive regions, whereas Fe/sub 3/B and Nd/sub 2/Fe/sub 14/B do not show stable passivation. Polymer-bonded magnets of different compositions have a significantly improved resistance toward strongly acidic environments as compared to hot pressed magnets. Enrichment in Fe content and additions like Co and Nb improve their corrosion behavior.

Resonance Rayleigh scattering method for the recognition and determination of double-stranded DNA using amikacin

In weakly acidic buffer medium, the interaction of amikacin with calf thymus DNA, yeast RNA and denatured DNA has been investigated by using resonance Rayleigh scattering (RRS) technique. The result shows that calf thymus DNA is capable of enhancing the RRS intensity of the amikacin, while yeast RNA and denatured DNA have very little enhancement effect. Based on the characteristics, a sensitive assay for detecting double-stranded DNA in the presence of denatured DNA and yeast RNA has been developed. The enhancement of the RRS signal is directly proportional to the concentration of double-stranded DNA in the range 0.02–12.0 μg ml −1 for calf thymus DNA and its detection limit (3 σ) is 2.5 ng ml −1. The method shows a wide linear range and high sensitivity, and almost no interference can be observed from RNA, denatured DNA, amino acid and most of the metal ions. The trace amounts of nucleic acid in synthetic samples and practical samples are determined with satisfactory results. Therefore, the proposed method is promising for as an effect means for recognition in vivo and determination in situ of double-stranded DNA.

Acid-base analysis during experimental anemia in rats

The present study evaluated the acid-base status of anemic rats by using two approaches of acid-base analysis: one based on the base excess (BE) calculation and the other based on Stewart's physicochemical analysis. Two sets of experimental data, derived from two different methods of inducing anemia, were used: repetitive doses of phenylhydrazine (PHZ) and bleeding (BL). A significant uncompensated respiratory alkalosis was found in both groups of anemic rats. BE increased slightly, whereas strong ion difference ([SID]) and weak acid buffers ([A(TOT)]) remained unchanged in anemic rats. The reasons for the absence of compensation for hypocapnia and the differences in the behaviour of acid-base variables are discussed. BE increase was considered paradoxical; its calculation was affected by the experimental conditions and BE had little physiological relevance during anemia. The absence of metabolic renal compensation in anemic rats could be due to a lower pH in the kidney due to anemic hypoxia. Finally, the changes in buffer strength related to low Hb and low P(CO2) might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.

PH(i) responses to osmotic cell shrinkage in the presence of open-system buffers.

Changes in plasma volume in vivo cause rapid changes in extracellular pH by altering the plasma bicarbonate concentration at a constant Pco(2) (Garella S, Chang BS, and Kahn SI. Kidney Int 8: 279, 1975). Few studies have examined the possibility that changes in cell volume produce comparable changes in intracellular pH (pH(i)). In the present study, alveolar macrophages were exposed to hyperosmotic medium in the absence or presence of the open-system buffers CO(2)-HCO(3)(-), propionic acid-propionate, or NH(3)-NH(4)(+). In the absence of open-system buffers, exposure to twice-normal osmolarity (2T) produced a slow cellular alkalinization [change in pH(i) (DeltapH(i)) approximately 0.38; exponential time constant (tau) approximately 120 s]. In the presence of 5% CO(2), 2T caused a biphasic pH(i) response: a rapid increase (DeltapH(i) approximately 0.10, tau approximately 15 s) followed by a slower pH(i) increase. Identical rapid pH(i) increases were produced by 2T in the presence of propionic acid (20 mM). Conversely, 2T caused a rapid pH(i) decrease (DeltapH(i) approximately -0.21, tau approximately 10 s) in the presence of NH(3) (20 mM). Thus osmotic cell shrinkage caused rapid pH(i) changes of opposite direction in the presence of a weak acid buffer (contraction alkalosis with CO(2) or propionic acid) vs. a weak base buffer (contraction acidosis with NH(3)). Graded DeltapH(i) were produced by varying extracellular osmolarity in the presence of open-system buffers; osmolarity increases of as little as 5-10% produced significant DeltapH(i). The rapid pH(i) responses to 2T were insensitive to inhibitors of membrane H(+) transport (ethylisopropylamiloride and bafilomycin A(1)). The results are consistent with shrinkage-induced disequilibria in the total cellular buffer system (i.e., intrinsic buffers plus added weak acid-base buffer).

Acid-base analysis during experimental anemia in rats

The present study evaluated the acid-base status of anemic rats by using two approaches of acid-base analysis: one based on the base excess (BE) calculation and the other based on Stewart's physicochemical analysis. Two sets of experimental data, derived from two different methods of inducing anemia, were used: repetitive doses of phenylhydrazine (PHZ) and bleeding (BL). A significant uncompensated respiratory alkalosis was found in both groups of anemic rats. BE increased slightly, whereas strong ion difference ([SID]) and weak acid buffers ([A(TOT)]) remained unchanged in anemic rats. The reasons for the absence of compensation for hypocapnia and the differences in the behaviour of acid-base variables are discussed. BE increase was considered paradoxical; its calculation was affected by the experimental conditions and BE had little physiological relevance during anemia. The absence of metabolic renal compensation in anemic rats could be due to a lower pH in the kidney due to anemic hypoxia. Finally, the changes in buffer strength related to low Hb and low P(CO2) might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.

CURRENT STATUS OF ACID-BASE QUANTITATION IN PHYSIOLOGY AND MEDICINE

Acid-base balance (ABB) is best determined by measurements in arterial whole blood, but for clinical purposes it can be expressed as estimated to apply to the entire extracellular fluid (ECF) of the body. ABB is determined by three independent variables: (1) respiratory (P co2); (2) metabolic (strong ion difference [SID]); (3) nonvolatile weak acid buffer (ATOT), primarily hemoglobin (Hb). Here we describe and compare four current indices of the metabolic component: (1) Standard base excess (SBE), in mM⋅L–1, quantifies the metabolic component, by assuming that the mean buffer strength of the ECF in humans equals that of blood with 5 g/dL hemoglobin. Despite individual variation of hemoglobin, the effective ATOT of ECF in vivo is practically invariant. SBE is automatically computed by most blood gas analyzers from P co2 and pH. (2) SID between plasma strong cations and anions, numerically equal to buffer base, as modified to apply to ECF in vivo. (3) HCO3– calculated from pH and P co2. Because pH and HCO3– vary with both P co2 and SID, equations are needed when this method is used to compare the sample with the usual or expected compensation for an ABB abnormality. Such computations do not produce a measure of the metabolic component. (4) Anion gap, Na+ + K+ − Cl– − HCO3–, detects anions not normally measured by plasma electrolyte screens. It can distinguish acidosis due to excess Cl– from that of other strong anions such as lactate. Using published pH (or H+) and HCO3– data, we have computed the typical compensatory responses of patients with primary acid-base imbalances in terms of SBE and Pa co2:

On‐column sample concentration of high‐ionic‐strength samples in capillary electrophoresis

High-ionic-strength samples result in poor electrophoretic separation efficiencies due to “destacking” of the sample. A simple method is described to stack high-ionic-strength samples without matrix modification prior to injection. Using a weak-acid buffer such as acetate as the background electrolyte, the electrokinetic injection of the sample is immediately followed by electrokinetic injection of an acid solution. The resulting titration of the background electrolyte produces a low-conductivity zone across which sample cations are focused. A sevenfold sensitivity enhancement was achieved with improved separation efficiency relative to normal electrokinetic injection. © 1998 John Wiley & Sons, Inc. J Micro Sep 10: 511–517, 1998

On-column sample concentration of high-ionic-strength samples in capillary electrophoresis

High-ionic-strength samples result in poor electrophoretic separation efficiencies due to “destacking” of the sample. A simple method is described to stack high-ionic-strength samples without matrix modification prior to injection. Using a weak-acid buffer such as acetate as the background electrolyte, the electrokinetic injection of the sample is immediately followed by electrokinetic injection of an acid solution. The resulting titration of the background electrolyte produces a low-conductivity zone across which sample cations are focused. A sevenfold sensitivity enhancement was achieved with improved separation efficiency relative to normal electrokinetic injection. © 1998 John Wiley & Sons, Inc. J Micro Sep 10: 511–517, 1998

Components of the blood acid-base disturbance that accompanies urethane anaesthesia in rats during normothermia and hypothermia.

1. We have studied the components of the metabolic acidosis that accompanies urethane anaesthesia in rats, both with and without the hypothermia that results from this anaesthesia. 2. Acid-base disturbances were analysed with an approach based on Stewart's analysis of acid-base chemistry. 3. The pH fall in the blood of normothermic anaesthetized rats (body temperature Tb) = 37 degrees C) was related to increases in plasma anions (lactate and [Cl-]), which decreased the strong ion difference ([SID]), as well as to increase the weak acid buffers due to increases in albumin. 4. A stronger metabolic acidosis was found in the blood of rats with hypothermia induced by urethane (Tb = 32 degrees C). Although plasma lactate was unchanged in hypothermic rats, [SID] decreased due to alterations in the plasma ionic balance. The metabolic acidosis found in hypothermia was also associated with increased weak acid buffers due to increases in albumin and inorganic phosphate. Further to hyperphosphataemia, signs of acute renal disfunction, such as increases in plasma [Mg2+] and blood urea nitrogen were found. Plasma retention of endogenous acids together with the retention of acid end-products of the metabolism of urethane because of acute renal failure may have contributed to strengthening the fall in pH and [HCO3-] found in urethane-induced hypothermic rats.

Sugar release from maize coleoptiles during auxin-, fusicoccin- and acid-mediated elongation growth

Summary The biochemical mechanism of the cell wall-loosening process underlying auxin-induced elongation growth of plant organs is still unresolved. A hypothesis currently under debate states that the breakdown of cell-wall polysaccharides by hydrolytic enzymes (cell-wall autolysis) is involved in this process. In order to test this hypothesis we have investigated the release of soluble carbohydrates by maize coleoptile segments during the initial period of the growth responses induced by auxin (indole-3-acetic acid), fusicoccin, and weak acidic buffer (pH 4). As previously shown for isolated cell walls (Hohl et al., 1991), abraded segments release monomeric, oligomeric and polymeric carbohydrates into the incubation medium. No other monosaccharides besides glucose could be detected in these fractions after hydrolysis, indicating that no non-glucan polysaccharides are involved in this process. Auxin had no effect on carbohydrate release in vivo. Also under conditions of acid-mediated growth in the presence of pH-4 buffer, no pH-dependent enhancement of carbohydrate release could be detected although buffer per se (pH 4 to 7) had a stimulating effect. Fusicoccin increased carbohydrate release but this effect may not be caused by cell-wall acidification. In contrast to auxin, fusicoccin had no effect on cell-wall extensibility measured in terms of load-extension curves (hysteresis loops) of killed segments. We conclude from these results that, although autolysis of cell-wall polysaccharides takes place in the growing tissue, it is not causally involved in the control of growth.

Base excess] and [strong ion difference] during O2-CO2 exchange.

Detecting uptake or production of "metabolic acid" by a given tissue is often of interest. [Base excess] ([BE]) is the change in [strong acid] or [strong base] needed to restore pH to normal at normal PCO2. However, [BE] seems to have the potential for minor inaccuracy during hypercarbia, and venous blood is hypercarbic relative to arterial. Another approach is [strong ion difference] ([SID]), where a strong ion is one that is always dissociated in solution, and where [SID] = [strong cation] - [strong anion]. The hypothesis was tested that a-v [SID]p might be used to detect metabolic acid uptake or production by tissue. A computer simulation of O2-CO2 exchange was performed, using the Siggaard-Andersen [BE] equations, which provide an existing conceptual template. It was assumed that a change in [BE] = a change in [SID] (Adv. Exp. Med. Biol., in press). (A-v) [SID]p decreased linearly with decreasing [HbO2] during equimolar O2-CO2 exchange (delta mEq [SID]p.l-1 per delta gHbO2.dl-1 = 0.6, r2 = 1.0), and erythrocyte [BE] ([BE]e) and [SID]e decreased commensurately, such that [BE]WB remained constant. These changes represent ion exchanges between erythrocyte and plasma, governed by the Gibbs-Donnan equilibrium. It is concluded that a-v [SID]p may be used to examine a-v differences in [metabolic acid], based in [BE] concepts. The concentration of "metabolic acid" ([metabolic acid]) in blood increases during endotoxemia, exercise and shock. To identify organ(s) responsible, it is necessary to measure arteriovenous [strong acid]. Two methods are available. Whole blood base excess ([BE]WB), is the change in [strong acid]WB or [strong base]WB needed to restore plasma pH (pHp) to 7.4 at PCO2 of 40 torr, and is an excellent method for distinguishing "respiratory," from "metabolic" acidosis in arterial blood. However, while [BE] is most helpful conceptually, use of [BE] in venous blood presents two problems. First, [BE]WB may employ in vitro assumptions that are slightly inaccurate during hypercarbia in vivo, and venous blood is hypercarbic relative to arterial. The problem seems to be that [BE] assumes greater [hemoglobin] ([Hb]) than is actually effective in vivo, where Hb is diluted in the extracellular volume. The "Van Slyke" version of the [BE]WB equation is: BE]WB = ¿[HCO3-]p - 24.4 + (2.3 x [Hb] + 7.7) x (pHp - 7.4)¿ x (1-0.023 x [Hb]) (1) This equation may be thought of conceptually as: [BE] = ([HCO3-] + [A-]) - (normal [HCO3-] + normal [A-]) (2) where A- is negatively charged non-volatile weak acid. Missing or excess charges are attributed to abnormal [strong acid] or [strong base], and [A-]WB is computed using actual, as opposed to effective, [Hb]. This problem has been adequately addressed in arterial blood by standard [BE]WB ([SBE]WB), by assuming that effective [Hb] in vivo is approximately one third of that in vitro. However, it is not clear whether this assumption is sufficiently accurate to examine arteriovenous differences. A second and related problem with using [BE] to detect (a-v) differences is the magnitude of change in Hb buffering in vivo during O2 desaturation. Desaturation renders Hb a stronger weak acid buffer, i.e. increases its effective pK value. Consequently, [HCO3-]p is greater at any given PCO2, creating the appearance of a larger [BE]WB, whereas [strong acid] or [strong base] has not changed. This artifact can be corrected using the "O2 desaturation transform factor," which is 0.19 mM delta g [HbO2].dl-1 in vitro. In vivo, however, the magnitude of the O2 desaturation transform factor might be different. An alternative approach to acid-base analysis is strong ion difference (SID) where a strong ion is one that is always dissociated in physiologic solution. [SID] can usually be approximated as: [Na+] + [K+] - [Cl-] - [La-]. Although [BE] does not equal [SID], a change in [BE] must always accompany a change in [SID], and vice-versa. While the [SID] approach is tedious, and often unnecessarily so, [SID] ca

A physical–chemical analysis of the acid–base response to chronic obstructive pulmonary disease

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.

Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats.

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.

Modelling chloride and CO 2 chemistry in the wairakei geothermal reservoir

The chloride and CO 2 chemistry of the Wairakei geothermal field, New Zealand, has been modelled using an extended version of the geothermal simulator TOUGH2. This version of the simulator solves the equations for the transport of reacting chemical species in multi-phase fluids, and is applied here to a detailed, full-scale geothermal reservoir model for the first time. Reactions involving the speciation of CO 2 to H 2CO 3 and HCO 3 − are included in the model, as is the “Henry's Law” reaction for exsolution of aqueous CO 2 to the vapour phase. Because CO 2 speciation in water is pH dependent, a reaction involving the most important weak acid buffer at Wairakei (H 4SiO 4) has also been included in the model. The chloride is treated as a conservative, non-reacting species that is present only in the liquid phase. Results from the model compare favourably with measured chloride and CO 2 data from Wairakei covering the period 1959–1987.

Blood acid–base changes during acute experimental inflammation in rats

Acidosis has often been reported in inflamed tissues, and changes in strong relevant ions at the site of inflammation may provoke alterations in blood acid-base status. We measured changes in blood acid-base variables during carrageenan-induced inflammation in rats. We found a mixed acid-base disorder in rat blood during acute inflammation (12, 24, and 48 h). A metabolic acid contribution was found during the first 12 h and maintained further, as revealed by a decrease in plasma strong ion concentration difference ([SID]) and an increase in plasma weak acid concentration due to a rise in inorganic phosphate ([ATOT]P(i)). Plasma [SID] and [ATOT]P(i) changes were probably due to exchange of Na+ and P(i) between the inflammatory exudate and rat blood. A secondary respiratory compensation for the metabolic acid changes occurred in the blood of inflamed rats, resulting in significant hypocapnia. Furthermore, a progressive decrease in the total weak acid buffer concentration due to a decrease in plasma albumin ([ATOT]Alb) also counteracted the impact of changes in [SID] and P(i) to increase blood acidity. Therefore, despite the metabolic acid-base disorders induced by inflammatory processes, hydrogen ion (H+) homeostasis was maintained, and blood pH remained essentially unchanged in the inflamed rats.

Perivitelline Fluid pH of Rainbow Trout (Oncorhynchus mykiss) Eggs in Relation to Ambient pH

In soft water of various pH levels, the perivitelline fluid of late eyed rainbow trout (Oncorhynchus mykiss) eggs showed significant pH buffering: final perivitelline pH was higher than ambient by 0.7–0.85 pH unit in acidified water but was lower by 0.3–1.0 pH unit in weak acidified or basic water. No significant difference between the pH of an external buffer solution and that of the perivitelline fluid could be observed after 24 h. Most rapid perivitelline pH change occurred in the first 2 h and in the first 10–20 min, when eggs were transferred from acidified to weak acid or basic water and buffer, respectively. Final pH of the perivitelline fluid was reached after 48 h in unbuffered water and 24 h or less in buffer.