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Biochemistry of Buffering Capacity and Ingestion of Buffers In Exercise and Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Bryan Saunders, Guilherme G. Artioli, Eimear Dolan, Rebecca L. Jones, Joseph Matthews, Craig Sale
These findings question the efficacy and mechanism of action of sodium citrate. A possible explanation is that an inhibitory effect of increased intracellular citrate counteracts the increase in extracellular buffering capacity (62). Citrate can allosterically inhibit the rate-limiting glycolytic enzyme, phosphofructokinase, and thus reduce adenosine triphosphate production. A further issue could be the timing of ingestion, since most studies included in the meta-analysis supplemented sodium citrate 90 to 120 minutes prior to exercise (16). As discussed, this may be a sub-optimal strategy as it does not allow for peak blood alkalosis and coincides with greater side effects (124). Thus, improvements in exercise performance may be more apparent with a longer period between sodium citrate ingestion and the start of the task, but this remains to be experimentally confirmed.
Urolithiasis
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Thomas Johnston, James Armitage, Oliver Wiseman
Urinary alkalinisation is important in the management of patients with both cystine stones and uric acid calculi. Sodium bicarbonate and potassium citrate are commonly used agents. Sodium bicarbonate is taken by mouth (325 to 2000 mg orally 1 to 4 times a day) and the dose titrated according to response. Common side effects include bloating and flatulence, but it may lead to salt and water retention and can worsen hypertension. The high sodium intake can lead to increased calcium absorption from the bowel and may increase the risk of calcium oxalate stones. Potassium citrate solution (10–20 mL three times per day) is again titrated according to urinary pH. It has a foul taste and compliance is less than 50%. Potassium citrate tablets are an alternative but are not available in the United Kingdom. Sodium citrate may also be used as a more palatable alternative. The target pH reflects the pKa of the stone constituents (for example, cystine – pKa 8.3, urate – pKa 5.8).
Buffering agents
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
Lars R McNaughton, Cameron Brewer, Sanjoy Deb, Nathan Hilton, Lewis Gough, Andy Sparks
Traditionally, sodium citrate has been ingested in a dose of 500 mg·kg-1 BM, between 90 and 120 min prior to exercise (77). That has been mooted as a physiologically optimal dose to increase the level of alkalosis (pH and HCO3-) to the required level to improve exercise performance. Early research by McNaughton (67) identified 500 mg·kg-1 BM sodium citrate was significantly more effective at improving 60-second maximal cycling exercise compared to lower doses (100, 200, 300 and 400 mg·kg-1 BM), when ingested 90 min prior to exercise in fluid form. Since this seminal work however, consistent positive effects on performance have failed to be produced, as Carr et al. (23) showed an unclear 0.0 ± 1.3% improvement within a meta-analysis of 15 studies. This lack of effect may explain the lack of research interest in sodium citrate in recent periods, in comparison to other buffering agents, such as NaHCO3 and β-alanine (51, 70).
Acid–base balance in hemodialysis patients in everyday practice
Published in Renal Failure, 2022
Monika Wieliczko, Jolanta Małyszko
Despite the improvement in hemodialysis techniques, acid–base balance still remains a challenge, there is a huge discrepancy between recommendation publishes several years ago and real-world data. New guidelines how to correct acid–base disorders in hemodialysis patients are needed to have less ‘acidotic’ patients before hemodialysis and less ‘alkalotic’ patients after the session. Currently, no studies are available addressing this issue. It appears that individualization of the standard HD session would be of value, however, we need more large-scale studies to prove or disprove this hypothesis [11]. A change in dialysate content or a bicarbonate profiling could also be considered as an option. Sodium bicarbonate supplementation therapy could also be taken into account as reported Kourtellidou et al. in randomized controlled trial [38]. Although alkali treatment (sodium citrate or sodium bicarbonate) would be helpful, we should remember that this type of intervention is not free from side effects. Sodium citrate can lead to increase gastric aluminum absorption and sodium bicarbonate—to bloating and flatulence [39–41].
Clot activators and anticoagulant additives for blood collection. A critical review on behalf of COLABIOCLI WG-PRE-LATAM
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
G. Lima-Oliveira, L. M. Brennan-Bourdon, B. Varela, M. E. Arredondo, E. Aranda, S. Flores, P. Ochoa
Sodium citrate is commonly used as a solution of dihydrate trisodium citrate. It is a nontoxic anticoagulant that converts Ca++ ions to the non-ionized form and prevents coagulation (Figure 4) [92]. In the clinical laboratory, it is employed mainly for preventing blood coagulation for hemostasis testing, platelet studies, and erythrocyte sedimentation rate. While additives may be liquid or dry, the latter form is preferable because the water of the liquid additives can diffuse out the plastic and jeopardize the blood/additive ratio. However, buffered sodium citrate is available only in liquid form. Therefore, manufacturers of evacuated tubes have developed a “double wall” tube system to avoid water loss and to maintain the quality of their product. Briefly the sodium citrate used in evacuated tubes has a pH ∼ 5.8 that requires approximately −40 °C in the crystallization phase of lyophilization, making the process of lyophilization of this additive in evacuated tubes impractical [93].
Evaluation of an in vitro coronary stent thrombosis model for preclinical assessment
Published in Platelets, 2020
Dylan Perry-Nguyen, Richard G. Jung, Alisha Labinaz, Anne-Claire Duchez, Omar Dewidar, Trevor Simard, Denuja Karunakaran, Kamran Majeed, Kiran Sarathy, Ruonan Li, F. Daniel Ramirez, Pietro Di Santo, Rebecca Rochman, Derek So, Nicolas Foin, Benjamin Hibbert
In order to determine the optimal content of sodium citrate, blood from volunteers was collected in 1%, 2%, and 3% sodium citrate tubes and incubated for 15 min prior to analysis. Thrombus burden was significantly larger with blood collected in 1% as opposed to 2% and 3% citrate tubes (20.5 ± 3.1%; n = 16, 5.6 ± 0.5%; n = 6, and 8.1 ± 2.0%; n = 8, for 1%, 2% and 3%, respectively, p < 0.01, Figure 2A). Blood collected in 0% sodium citrate tubes thrombosed prior to running the assay and were excluded from the analysis. Furthermore, activated clotting times did not differ between 0%, 1%, and 3% sodium citrate tubes (Supplemental Figure 1). Secondarily, perfusion time was optimized targeting 20–80% clot formation. Samples with 1% citrate were run for 10, 15, and 20 min prior to analysis of thrombus burden by OCT. An increase in thrombus burden was observed as perfusion duration increased from 10 to 20 minutes (7.4 ± 1.8%; n = 7, 20.5 ± 3.1%; n = 16, and 23.7 ± 3.2%; n = 7, for 10, 15, and 20 min, respectively, p = 0.01, Figure 2B). Thrombus burden stabilized at 20 min with no significant progression from 15 min.