Daily variation in plasma electrolyte and acid–base status in fasted horses over a 25 h period of rest

2006 ◽  
Vol 3 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger
Keyword(s):  
Time Course ◽  
Daily Variation ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Night Time ◽  
Plasma Protein Concentration ◽  
Plasma Electrolyte ◽  
Acid Base Status

AbstractMeasurement and interpretation of acid–base status are important in clinical practice and among racing jurisdictions to determine if horses have been administered alkalinizing substances for the purpose of enhancing performance. The present study used the physicochemical approach to characterize the daily variation in plasma electrolytes and acid–base state that occurs in horses in the absence of feeding and exercise. Jugular venous blood was sampled every 1–2 h from two groups (n=4 and n=5) of Standardbred horses over a 25 h period where food and exercise were withheld. One group of horses was studied in October and one in December. The time course and magnitude of circadian responses differed between the two groups, suggesting that subtle differences in environment may manifest in acid–base status. Significant daily variation occurred in plasma weak acid concentration ([Atot]) and strong ion difference ([SID]), [Cl−], [K+], [Na+] and [lactate−], which contributed to significant changes in [H+] and TCO2. The night-time period was associated with a mild acidosis, marked by increases in plasma [H+] and decreases in TCO2, compared with the morning hours. The night-time acidosis resulted from an increased plasma [Atot] due to an increased plasma protein concentration ([PP]), and a decreased [SID] due to increases in [Cl−] and decreases in [Na+]. An increased plasma [K+] during the night-time had a mild alkalotic effect. There were no differences in pCO2. It was concluded that many equine plasma electrolyte and acid–base parameters exhibit fluctuations in the absence of feeding and exercise, and it is likely that some of these changes are due to daily variation.

Cyclical plasma electrolyte and acid–base responses to meal feeding in horses over a 24-h period

2005 ◽  
Vol 2 (3) ◽  
pp. 159-169 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger
Keyword(s):  
Time Course ◽  
Venous Blood ◽  
Weak Acid ◽  
Minor Effect ◽  
Acid Base ◽  
Plasma Electrolyte ◽  
Cyclical Fluctuations ◽  
Base Parameters ◽  
Acid Protein ◽  
A Minor

AbstractThe present study used the physicochemical approach to characterize the changes in plasma electrolyte and acid–base states that occur in horses in response to feeding. Jugular venous blood was sampled every 0.5–2 h over a 24-h period from two groups (n = 4 and n = 5) of Standardbreds fed a mixed hay and grain ration at 8 am and 7 pm. One group of horses was studied in October, and one in December. The time course and magnitude of feeding responses differed between groups, and between the morning and evening meals. Feeding-induced changes in plasma electrolyte and acid–base variables occurred rapidly, within the first 1–3 h of meal consumption. The plasma acidosis associated with eating the meal was marked by increased plasma [H+] and decreased TCO2. The primary contributors to the increases in plasma [H+] were the decrease in the plasma concentration of strong ions ([SID]) and the pCO2. The increase in plasma total weak acid (protein) concentration ([Atot]) post-feeding had only a minor effect on the acid–base state. The feeding-induced acidosis abated 3–6 h after the meal, showing cyclical recovery of physicochemical variables that contributed to the acid–base disturbance. It is concluded that several key plasma electrolyte and acid–base parameters undergo significant, cyclical fluctuations in response to feeding in horses.

scholarly journals Responses of a Stenohaline Freshwater Teleost (Catostomus Commersoni) to Hypersaline Exposure: I. The Dependence of Plasma pH and Bicarbonate Concentration on Electrolyte Regulation

1986 ◽  
Vol 121 (1) ◽  
pp. 77-94 ◽  
Author(s):  
P. R. H. WILKES ◽  
B. R. MCMAHON
Keyword(s):  
Plasma Concentrations ◽  
Haemoglobin Concentration ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Catostomus Commersoni ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Plasma Electrolyte ◽  
Acid Base Status

The effects of exposure to 0.94% (300 mosmol1−1) sodium chloride on plasma electrolyte and acid-base status were examined in the freshwater stenohaline teleost Catostomus commersoni (Lacépède), the white sucker. Four days' exposure to this maximum sublethal salinity resulted in an increase in plasma concentrations of both sodium and chloride but a decrease in the Na+/Cl− ratio. Since the plasma concentrations of free amino acids and other strong ions - Ca2+, Mg2+ and K+ - remained unchanged, plasma strong ion difference (SID) decreased. Additionally, plasma pH and bicarbonate concentration decreased at constant Pcoco2 The changes in electrolyte and acid-base status that occurred after the 96 h were not appreciably altered after a further 2–3 weeks of saline exposure. The ambient calcium concentration had no influence on these results. Haemolymph non-bicarbonate buffer capacity (β) calculated as Δ[HCO3−]/ ΔpH, increased in saline-exposed fish. Consequently ΔH+, the apparent proton load, was zero despite the apparent change in acid-base status. Although β was directly proportional to the haemoglobin concentration in both control and experimental fish, this could not account for the increase in β since haemoglobin remained at control values. These results can be explained solely by the change in plasma SID and serve to illustrate the dependence of plasma acid-base status on the prevailing electrolyte characteristics, weak acid concentration and Pcoco2.

scholarly journals Hypoproteinemia, strong-ion difference, and acid-base status in critically ill patients

1998 ◽  
Vol 84 (5) ◽  
pp. 1740-1748 ◽  
Author(s):  
Peter Wilkes
Keyword(s):  
Total Protein ◽  
Protein Concentration ◽  
Total Concentration ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Acid Base Status ◽  
The Relationship

The present study was a prospective, nonrandomized, observational examination of the relationship among hypoproteinemia and electrolyte and acid-base status in a critical care population of patients. A total of 219 arterial blood samples reviewed from 91 patients was analyzed for arterial blood gas, electrolytes, lactate, and total protein. Plasma strong-ion difference ([SID]) was calculated from [Na+] + [K+] − [Cl−] − [La−]. Total protein concentration was used to derive the total concentration of weak acid ([A]tot). [A]tot encompassed a range of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with [A]tot. The decline in [SID] was primarily attributable to an increase in [Cl−]. A direct correlation was also noted between[Formula: see text] and [SID], but not between [Formula: see text] and [A]tot. The decrease in [SID] and [Formula: see text] was such that neither [H+] nor [[Formula: see text]] changed significantly with [A]tot.

Equivalent Metabolic Acidosis with Four Colloids and Saline on Ex Vivo Haemodilution

2009 ◽  
Vol 37 (3) ◽  
pp. 407-414 ◽  
Author(s):  
T. J. Morgan ◽  
M. Vellaichamy ◽  
D. M. Cowley ◽  
S. L. Weier ◽  
B. Venkatesh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Base Excess ◽  
Ex Vivo ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Acid Properties

Colloid infusions can cause metabolic acidosis. Mechanisms and relative severity with different colloids are incompletely understood. We compared haemodilution acid-base effects of 4% albumin, 3.5% polygeline, 4% succinylated gelatin (all weak acid colloids, strong ion difference 12 mEq/l, 17.6 mEq/l and 34 mEq/l respectively), 6% hetastarch (non-weak acid colloid, strong ion difference zero) and 0.9% saline (crystalloid, strong ion difference zero). Gelatin weak acid properties were tracked via the strong ion gap. Four-step ex vivo dilutions of pre-oxygenated human venous blood were performed to a final [Hb] near 50% baseline. With each fluid, base excess fell to approximately −13 mEq/l. Base excess/[Hb] relationships across dilution were linear and direct (R2 ≥0.96), slopes and intercepts closely resembling saline. Baseline strong ion gap was −0.3 (2.1) mEq/l. Post-dilution increases occurred in three groups: small with saline, hetastarch and albumin (to 3.5 (02) mEq/l, 4.3 (0.3) mEq/l, 3.3 (1.4) mEq/l respectively), intermediate with polygeline (to 12.2 (0.9) mEq/l) and greatest with succinylated gelatin (to 20.8 (1.4) mEq/l). We conclude that, despite colloid weak acid activity ranging from zero (hydroxyethyl starch) to greater than that of albumin with both gelatin preparations, ex vivo dilution causes a metabolic acidosis of identical severity to saline in each case. This uniformity reflects modifications to the albumin and gelatin saline vehicles, in part aimed at pH correction. By proportionally increasing the strong ion difference, these modifications counter deviations from pure saline effects caused by colloid weak acid activity. Extrapolation in vivo requires further investigation.

Physicochemical analysis of acid–base status during recovery from high-intensity exercise in Standardbred racehorses

2005 ◽  
Vol 2 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Amanda Waller ◽  
Michael I Lindinger
Keyword(s):  
High Intensity ◽  
Venous Blood ◽  
Physicochemical Analysis ◽  
High Intensity Exercise ◽  
Ion Concentration ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Acid Base Status ◽  
Standardbred Racehorses

AbstractThe present study used the physicochemical approach to characterize the changes in acid–base status that occur in Standardbred racehorses during recovery from high-intensity exercise. Jugular venous blood was sampled from nine Standardbreds in racing condition, at rest and for 2 h following a high-intensity training workout. Plasma [H+] increased from 39.1±1.0 neq l−1 at rest to 44.8±2.7 neq l−1 at 1 min of recovery. A decreased strong ion difference ([SID]) was the primary contributor to the increased [H+] immediately at the end of exercise, while increased plasma weak ion concentration ([Atot]) was a minor contributor to the acidosis. A decreased partial pressure of carbon dioxide (PCO2) at 1 min of recovery had a slight alkalinizing effect. The decreased [SID] at 1 min of recovery was a result of a 15.1±3.1 meq l−1 increase in [lactate−], as [Na+] and [K+] were also increased by 6.5±0.7 and 1.14±0.06 meq l−1, respectively, at 1 min of recovery. It is concluded that high-intensity exercise and recovery is associated with significant changes in acid–base balance, and that full recovery of many parameters that determine acid–base status requires 60–120 min.

Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans

1999 ◽  
Vol 276 (1) ◽  
pp. R32-R43 ◽  
Author(s):  
Michael I. Lindinger ◽  
Thomas W. Franklin ◽  
Larry C. Lands ◽  
Preben K. Pedersen ◽  
Donald G. Welsh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Plasma Electrolyte ◽  
Extracellular Compartment ◽  
Arterial Plasma ◽  
Male Subjects ◽  
Plasma Disturbance

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3 and KHCO3 ingestion. It was hypothesized that skeletal muscle is involved in the correction of the ensuing plasma disturbance by exchanging ions, gasses, and fluids between cells and extracellular fluids. Five male subjects, with catheters in a brachial artery and antecubital vein, ingested 3.57 mmol/kg body mass NaHCO3 or KHCO3. While seated, blood samples were taken 30 min before ingestion of the solution, at 10-min intervals during the 60-min ingestion period, and periodically for 210 min after ingestion was complete. Blood was analyzed for gases, hematocrit, plasma ions, and total protein. With NaHCO3, arterial plasma Na+ concentration ([Na+]) increased from 143 ± 1 to 147 ± 1 (SE) meq/l, H+ concentration ([H+]) decreased by 6 ± 1 neq/l, and [Formula: see text] increased by 5 ± 1 mmHg. There was no detectable net Na+ uptake by tissues. An increased plasma strong ion difference ([SID]) accounted fully for the decrease in plasma [H+]. With KHCO3, K+ concentration increased from 4.25 ± 0.10 to 7.17 ± 0.13 meq/l, plasma volume decreased by 15.5 ± 2.3%, [H+] decreased by 4 ± 1 neq/l, and there was no change in[Formula: see text]. The decrease in [H+] in the KHCO3 trial primarily arose in response to the increased [SID]. Net K+ uptake by tissues accounted for 37 ± 5% of the ingested K+. In conclusion, ingestion of NaHCO3and KHCO3 produced markedly different fluid and ionic disturbances and associated regulatory responses by skeletal muscle. Accordingly, the physicochemical origins of the acid-base disturbances also differed between treatments. The tissues did not play a role in regulating plasma [Na+] after ingestion of NaHCO3. In contrast, the net influx of K+ to tissues played an important role in removing K+ from the extracellular compartment after ingestion of KHCO3.

Acid–base regulations a comparison of quantitative methods

1994 ◽  
Vol 72 (7) ◽  
pp. 818-826 ◽  
Author(s):  
John M. Kowalchuk ◽  
Barry W. Scheuermann
Keyword(s):  
Quantitative Methods ◽  
Linear Regression Analysis ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Weak Acids ◽  
Acid Base ◽  
Ramp Exercise ◽  
The Difference ◽  
Biological Solutions

The [H+] and [HCO3−] of biological solutions is determined by the [Formula: see text], the concentration of strong ions (mainly Na+, K+, Ca2+, Cl−, lactate−), and the concentration of weak acids (mainly proteins, phosphates). Two mathematical models are available that use a quantitative approach to describe the acid–base behaviour of plasma, but which differ in their treatment of the weak acid component: Stewart model (using [Formula: see text], strong ion difference (SID = [Na+ + K+ + Ca2+] − [Cl− + lactate−]) and [protein]TOT); Fencl model (using [Formula: see text], SID, [albumin], and [Pi]TOT). The present study compared measured and estimated [H+] and [HCO3−] in whole-blood samples collected from eight subjects during two double-ramp exercise protocols to the limit of tolerance to assess the accuracy with which each of the quantitative models predicts measured values. Arterialized-venous blood was analyzed for [H+], [Formula: see text], [protein]TOT, [albumin], [Pi]TOT, and SID (= [Na+ + K+ + Ca2+] − [Cl− + lactate−]), and these independent variables were then substituted into the appropriate mathematical model to estimate [H+] and [HCO3−]. Analysis showed that the [H+] and [HCO3−] estimated using either model provided a good estimate of the [H+] (Stewart model, r = 0.81; Fencl model, r = 0.81) and [HCO3−] (Stewart model, r = 0.93; Fencl model, r = 0.93) measured in plasma; linear regression analysis demonstrated that the slopes and intercepts for each of die relationships were not different (p > 0.05) from the line of identity. Differences between estimated and measured values were small, averaging < 3 nmol∙L−1 for [H+] and < 2 mmol∙L−1 for [HCO3−]. However, in the case of plasma [H+], the difference between estimated and measured values became skewed (i.e., [H+]M < [H+]Est) above [H+]M ≈ 55 nmol∙L−1, or at [SID] ≤ 35 mequiv.∙L−1. Reasons for the difference between measured and estimated values are discussed, with attention given to the [SID] and weak acid components.Key words: quantitative acid–base chemistry, strong ion difference, weak acids, strong ions, lactate, hydrogen ion, bicarbonate.

Acid-base analysis during experimental anemia in rats

2000 ◽  
Vol 78 (10) ◽  
pp. 774-780 ◽  
Author(s):  
J Pesquero ◽  
V Alfaro ◽  
L Palacios
Keyword(s):  
Base Excess ◽  
Respiratory Alkalosis ◽  
Physicochemical Analysis ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Experimental Conditions ◽  
Physiological Relevance ◽  
Base Analysis ◽  
Acid Base Status

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 ([ATOT]) 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 Pc02 might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.Key words: anemia, phenylhydrazine, bleeding, base excess, strong ion difference, non-carbonic buffers.

Effect of menopause on the chemical control of breathing and its relationship with acid-base status

2009 ◽  
Vol 296 (3) ◽  
pp. R722-R727 ◽  
Author(s):  
Megan E. Preston ◽  
Dennis Jensen ◽  
Ian Janssen ◽  
John T. Fisher
Keyword(s):  
Venous Blood ◽  
Premenopausal Women ◽  
Weak Acid ◽  
Control Of Breathing ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Serum Progesterone ◽  
Sex Steroid Hormone ◽  
Peripheral Chemoreflex

This study examined the role of alterations in the chemoreflex control of breathing, acid-base balance, and their interaction in postmenopausal ventilatory adaptations. A modified iso-oxic hyperoxic and hypoxic CO2-rebreathing procedure was employed to evaluate central and peripheral chemoreflex drives to breathe, respectively, in 15 healthy postmenopausal and 20 premenopausal women of similar age. Arterialized venous blood samples were collected at rest for the estimation of arterial Pco2 (PaCO2) and H+ concentration ([H+]), plasma strong ion difference ([SID]) and total weak acid ([A]tot) concentrations, and serum progesterone ([P4]) and 17β-estradiol ([E2]) concentrations. In post- compared with premenopausal women, PaCO2, [SID], and the central chemoreflex ventilatory recruitment threshold for Pco2 (VRTco2) were higher, whereas [P4] and [E2] were lower (all P < 0.05), with no significant change in central or peripheral chemoreflex sensitivity, peripheral chemoreflex VRTco2, and [A]tot. The acidifying effect of an increased PaCO2 was offset by the alkalizing effect of an increased [SID], such that [H+] was preserved in post- compared with premenopausal women. PaCO2 correlated positively with the central chemoreflex VRTco2 ( r = 0.67, P < 0.01), which in turn correlated positively with [SID] ( r = 0.53, P < 0.01) within the pooled data. In conclusion, the relative alveolar hypoventilation and attendant arterial hypercapnia in healthy post- compared with premenopausal women could be explained, in part, by the interaction of 1) reduced central, but not peripheral, chemoreflex VRTco2, 2) increased [SID], and 3) reduced circulating female sex steroid hormone concentrations.

Total weak acid concentration and effective dissociation constant of nonvolatile buffers in human plasma

2001 ◽  
Vol 91 (3) ◽  
pp. 1364-1371 ◽  
Author(s):  
Peter D. Constable
Keyword(s):  
Dissociation Constant ◽  
Human Plasma ◽  
Total Concentration ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Horse Plasma ◽  
Using Data ◽  
Species Specific

The strong ion approach provides a quantitative physicochemical method for describing the mechanism for an acid-base disturbance. The approach requires species-specific values for the total concentration of plasma nonvolatile buffers (Atot) and the effective dissociation constant for plasma nonvolatile buffers ( K a), but these values have not been determined for human plasma. Accordingly, the purpose of this study was to calculate accurate Atot and K a values using data obtained from in vitro strong ion titration and CO2tonometry. The calculated values for Atot (24.1 mmol/l) and K a (1.05 × 10−7) were significantly ( P < 0.05) different from the experimentally determined values for horse plasma and differed from the empirically assumed values for human plasma (Atot = 19.0 meq/l and K a = 3.0 × 10−7). The derivatives of pH with respect to the three independent variables [strong ion difference (SID), Pco 2, and Atot] of the strong ion approach were calculated as follows: [Formula: see text] [Formula: see text], [Formula: see text]where S is solubility of CO2 in plasma. The derivatives provide a useful method for calculating the effect of independent changes in SID+, Pco 2, and Atot on plasma pH. The calculated values for Atot and K a should facilitate application of the strong ion approach to acid-base disturbances in humans.

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