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

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.

2006 ◽  
Vol 3 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger

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.


1972 ◽  
Vol 37 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Norval M. Simms ◽  
Don M. Long ◽  
James H. Matthews ◽  
Shelley N. Chou

✓ Oxygen tension and acid-base parameters of cerebral venous blood and cisternal cerebrospinal fluid, as well of femoral arterial blood, were studied in 14 dogs following injection of varying amounts of room air into the right vertebral artery. Acute elevations in oxygen tension were demonstrated in both cerebral venous blood and CSF, whereas hypoxemia occurred concomitantly in systemic arterial blood. Post-embolic increases in carbon dioxide tension with reciprocal diminutions in pH were evident in all sampling sites. The pathophysiological bases for these air-induced alterations are discussed.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Wing P. Chan ◽  
Fu-Chen Kung ◽  
Yu-Lin Kuo ◽  
Ming-Chen Yang ◽  
Wen-Fu Thomas Lai

A technique for synthesizing biocompatible hydrogels by cross-linking calcium-form poly(γ-glutamic acid), alginate sodium, and Pluronic F-127 was created, in which alginate can be cross-linked by Ca2+from Ca–γ-PGA directly andγ-PGA molecules introduced into the alginate matrix to provide pH sensitivity and hemostasis. Mechanical properties, swelling behavior, and blood compatibility were investigated for each hydrogel compared with alginate and forγ-PGA hydrogel with the sodium form only. Adding F-127 improves mechanical properties efficiently and influences the temperature-sensitive swelling of the hydrogels but also has a minor effect on pH-sensitive swelling and promotes anticoagulation. MG-63 cells were used to test biocompatibility. Gelation occurred gradually through change in the elastic modulus as the release of calcium ions increased over time and caused ionic cross-linking, which promotes the elasticity of gel. In addition, the growth of MG-63 cells in the gel reflected nontoxicity. These results showed that this biocompatible scaffold has potential for application in bone materials.


1982 ◽  
Vol 4 (4) ◽  
pp. 189-191
Author(s):  
P.G. van der Wal ◽  
H.G. Hulshof ◽  
G. van Essen ◽  
A. Meijering

2008 ◽  
Vol 99 (01) ◽  
pp. 169-173 ◽  
Author(s):  
Einor Ben Assayag ◽  
Irena Bova ◽  
Ludmila Shopin ◽  
Michael Cohen ◽  
Shlomo Berliner ◽  
...  

SummaryIncreased fibrinogen concentration is a well known phenomenon following acute ischemic stroke. However, the natural course of this hyperfibrinogenemia is uncertain. We aimed to clarify whether it is of a transient or more persistent nature in patients who harbor an underlying morbid biology of atherothrombo-inflammation. Venous blood for fibrinogen measurements was obtained from the control group participants and from stroke patients within 24 hours of admission, as well as 12 months following the acute event. In order to perform a time course analysis, we divided our cohort into tiles of time from symptoms' onset and compared the fibrinogen concentrations usingANOVA. Elevated fibrinogen concentrations were found in stroke patients on admission compared with matched controls (p<0.001).Analysis of variance in the different tertiles of time from symptoms' onset identified that fibrinogen concentrations were already relatively high during the initial phase of the event and did not differ significantly between the tiles (p=0.268). Moreover, when we calculated the absolute differences between the patients' fibrinogen concentrations and that of the matched controls there was clearly a minor increment during the time course from symptoms' onset in the stroke patients group. In conclusion, persistent hyperfibrinogenemia is present in patients with acute ischemic cerebral events and it might be present during the earlier stages of the disease as presently shown. Prompt and longterm, rather than short term, interventions to reduce the concentrations of this protein might therefore be of relevance.


2009 ◽  
Vol 37 (3) ◽  
pp. 407-414 ◽  
Author(s):  
T. J. Morgan ◽  
M. Vellaichamy ◽  
D. M. Cowley ◽  
S. L. Weier ◽  
B. Venkatesh ◽  
...  

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.


1999 ◽  
Vol 276 (1) ◽  
pp. R32-R43 ◽  
Author(s):  
Michael I. Lindinger ◽  
Thomas W. Franklin ◽  
Larry C. Lands ◽  
Preben K. Pedersen ◽  
Donald G. Welsh ◽  
...  

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.


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