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PubMed2001

The importance of glucose for the Escherichia coli mediated citrate depletion in synthetic and human urine.

OBJECTIVE: Escherichia coli has previously been shown to reduce urine citrate and influence urine pH. In this study the influence of glucose on the E. coli mediated citrate decrease has been investigated. MATERIAL AND METHODS: In synthetic urine, a glucose concentration of > or = 1 mmol/l was a prerequisite for bacteria to grow and lower citrate. At glucose concentrations > or = 5 mmol/l an E. coli mediated pH decrease correlated to urine glucose was observed. RESULTS: In human urine, variations in urine glucose influenced the citrate decrease and addition of glucose accelerated the E. coli mediated citrate decrease, which in certain urines could be very pronounced. CONCLUSIONS: Citrate has a pronounced effect on the activity product of calcium oxalate and calcium phosphate and the E. coli mediated decrease in urine citrate may be involved in the formation of urinary tract stones and catheter encrustations.

Citric Acid↗

PubMed2002

Urinary citrate excretion in idiopathic nephrolithiasis.

OBJECTIVE: To determine urinary citrate excretion in children with nephrolithiasis and normal controls. DESIGN: Prospective. SETTING: Tertiary care center in New Delhi. METHODS: This study was done on 50 children, below the age of 12 years, with idiopathic urinary calculi and 150 age and weight matched controls. The children were divided into 3 groups: Group 1 (1-4 years), Group 2 (5-8 years) and Group 3 (9-12 years). Urinary citrate was estimated in a 24-hour urine sample using colorimetric method. The stones removed from these children were also analysed. RESULTS: There was a preponderance of urinary stones in males; the highest incidence being in Group 1. Excretion of citrate in 24-hour urine sample was significantly lower in patients compared to controls, for males in all age groups and for females in Group 3. However, there was no statistically significant difference in the urinary citrate value between males and females in a given age group for either controls or patients. The urinary citrate excretion increased with age in patients and controls, but the levels in patients were lower. Depending upon the constituents, four types of stones were identified, calcium phosphate, calcium oxalate, uric acid and magnesium ammonium phosphate. Nine stones had at least more than one major constituent. Hypocitraturia was detected in 43 percent cases. The incidence was 76 percent for calcium phosphate, 87 percent for calcium oxalate, 40 percent for uric acid stones and 50 percent for magnesium ammonium phosphate. CONCLUSION: This study shows that low urinary citrate is associated with urinary stones in children, especially in endemic areas, in the absence of obvious etiological factors. Urinary citrate excretion should be determined in all children with nephrolithiasis.

Case-Control Studies↗

PubMed1980

Effect of shear rate on platelet interaction with subendothelium in citrated and native blood. II. Relationships among platelet adhesion, thrombus dimensions, and fibrin formation.

The adhesion of human platelets to subendothelium of rabbit aorta and the formation of microthrombi (aggregation) were investigated in an annular chamber after perfusion of native or citrated blood at wall shear rates ranging from 650 to 3300 sec-1. Previous studies demonstrated reduced adhesion and increased thrombi with native as compared to citrated blood and suggested that thrombi grow larger and higher in native blood. In the present study, thrombus dimensions were quantified by newly developed stereological techniques. The thrombus volume per surface area of subendothelium increased with increasing shear rate and was significantly greater in native blood. At 1300 sec-1 thrombi less than 5 and less than 10 micrometers in height were more frequent in citrated blood, and those greater than 20 micrometers were much more frequent in native blood. Maximum thrombus heights were 62 +/- 7 and 71 +/- 5 micrometers in native and 17 +/- 2 and 28 +/- 4 in citrated blood at shear rates of 650 and 1300 sec-1, respectively. Surface coverage with fibrin was 30%, 11%, and 0% at shear rates of 650, 1300, and 3300 sec-1, respectively. In addition, the effects of approximately 15 and approximately 45 mM citrate (final concentration in plasma) were studied at shear rates of 200, 650, and 2600 sec-1. At a citrate concentration of approximately 45 mM aggregation was abolished, and adhesion was strongly inhibited at the highest shear rate. We conclude that citrate (1) inhibits platelet attachment kinetics, thus acting to reduce adhesion, and (2) inhibits platelet aggregation and thrombus stability, thus reducing thrombus heights, which (3) may indirectly lead to increased adhesion.

Animals↗

PubMed1993

A prospective evaluation of clomiphene citrate challenge test screening of the general infertility population.

OBJECTIVE: To assess the results of screening an unselected general infertility population for diminished ovarian reserve with the clomiphene citrate challenge test. METHODS: Two hundred thirty-six couples were followed prospectively and studied for the relationship between clomiphene citrate challenge test screening and final diagnoses and long-term fertility rates. RESULTS: Abnormal clomiphene citrate challenge tests were found in two of 61 (3%) of the patients younger than 30 years, in five of 72 (7%) aged 30-34, in seven of 68 (10%) aged 35-39, and in nine of 35 (26%) aged 40 or older. An abnormal test predicted lower pregnancy rates; conception occurred in 92 of 213 (43%) of patients with normal results, but only two of 23 (9%) of patients with abnormal results (P < .004). Unexplained infertility (not considering the clomiphene citrate challenge test) was a common finding in patients with abnormal clomiphene citrate challenge test results (12 of 23). This incidence was significantly higher than that in patients with normal clomiphene citrate challenge test results (20 of 213) (P < .001). CONCLUSIONS: Approximately 10% of the patients in the general infertility population had abnormal clomiphene citrate challenge tests. The incidence of abnormal results increases with age beginning in the early 30s, occurs with a higher frequency in patients who would otherwise be diagnosed with unexplained infertility, and prognosticates decreased long-term pregnancy rates.

Adult↗

PubMed1998

Effect of oral aluminum and aluminum citrate on blood level and short-term tissue distribution of aluminum in the rat.

Aluminum (Al) absorption seems to be very low, but many factors can enhance it in animals and humans. In the present study, we investigated the acute effect of Na citrate on Al absorption by monitoring Al levels in blood and several tissues. For this purpose, 18 Wistar male rats were divided into 3 groups: control, Al, and Al + Na citrate. After a 14-h fasting period, animals were dosed orally with deionized water, or 2 mmol Al chloride, or 2 mmol Al chloride plus 2 mmol Na citrate. Blood samples were taken before and 1, 2, 4, and 6 h after the gavage. Al concentrations in blood, liver, tibia, kidney, and intestinal wall were determined by ICP-OES. In the Al and Al + citrate groups, Al blood concentrations peaked at 1 h and 2 h with higher levels in the Al + citrate group. Al gavage resulted in an increase in Al level in intestinal wall, but not in the other investigated tissues. Simultaneous gavage of citrate with Al significantly increased its tissue levels in tibia, kidney, and in intestinal wall. Our data show clearly that Al as chloride can be absorbed, but not well retained by the organism tissues. Furthermore, the model used in the present study is appropriate for acute studies to investigate the effect of various compounds on Al absorption in the rat.

Administration, Oral↗

PubMed2000

Dose-related elevations in venous pH with citrate ingestion do not alter 40-km cycling time-trial performance.

The purpose of the current investigation was to determine whether sodium citrate enhances endurance cycling performance and, if so, what dosage(s) produces this effect. Eight trained [peak power output: 362 (48) W; power:weight: 5.1 (0.4) W x kg(-1), mean (SD)] male cyclists were requested to complete four, 40-km time-trials, each separated by 3-7 days, on their own bicycles, mounted on a Kingcycle ergometer. To mimic the stochastic nature of cycle road races, the time-trials included four 500-m, four 1-km and two 2-km sprints. The experimental conditions involved the ingestion of three dosages of sodium citrate dissolved in 400 ml water: 0.2 g x kg(-1), 0.4 g x kg(-1) and 0.6 g x kg(-1) body mass (b.m.) and a placebo (calcium carbonate, 0.1 g x kg(-1) b.m.). Subjects were asked to complete both the sprints and total distance in the fastest time possible. Venous blood samples were collected before, as well as at 10-km intervals during the trials for the analysis of plasma lactate and glucose concentrations and for the measurement of blood pH and PCO2 levels. Immediately before, as well as during exercise, pH was significantly higher in the group ingesting the highest citrate dose (range 7.36-7.45) compared to the placebo (range 7.31-7.39) and the two lower citrate dosages. Despite this, no significant differences in power output (P = 0.886) or time taken to complete the 40 km (P = 0.754) were measured between the four trials. The average performance times (in min:s, with SD in parentheses) and average power output (in W) for the 40-km time-trials were: 58:46 (5:06) [265 (62) W], 60:24 (6:07) [251 (59) W], 61:47 (5:07) [243 (44) W] and 60:02 (5.05) [255 (55) W] for the 0.2, 0.4, 0.6 g x kg(-1) b.m. sodium citrate and placebo trials, respectively. There were also no significant differences measured between treatments in terms of time, power output, speed or heart rate during the 500-m, 1-km and 2-km sprints. The ingestion of increasing sodium citrate dosages before exercise produced dose-dependent changes in pH, base excess and HCO3- concentrations before and during the 40-km time-trial. However, these changes influenced neither the time-trial time nor the sprinting performance times.

Bicarbonates↗

PubMed1965

THE INCORPORATION OF CARBON DIOXIDE INTO MILK CITRATE IN THE ISOLATED PERFUSED GOAT UDDER.

1. Isolated perfused goat udders supplied with glucose, acetate and amino acids were infused for several hours with NaH(14)CO(3). 2. Lactose, milk-fat fatty acids and glycerol had very little radioactivity. The specific radioactivity (counts./min./mg. of C) of milk citrate was 9-16% that of the carbon dioxide in the perfusion fluid and 19% that estimated for tissue carbon dioxide. The specific radioactivity of tissue citrate resembled that of milk citrate. 3. The radioactivity in citrate was predominantly in C-6, suggesting some carboxylation of alpha-oxoglutarate in addition to carboxylation of C(3) compounds. 4. [1-(14)C]Glutamate was infused in a similar experiment, and milk citrate radioactivity was predominantly in C-1+C-5. 5. The results are discussed in relation to the contribution of glucose and acetate carbon to citrate. The implications of the carboxylation of alpha-oxoglutarate are considered.

Acetates↗

PubMed2003

Effect of 3.2 vs. 3.8% sodium citrate concentration on anti-Xa levels for patients on therapeutic low molecular weight heparin.

In this study, we compared the effect of sodium citrate, a sample collection variable, on the anti-Xa levels of patients (n = 28) on dalteparin, a low molecular weight heparin. The median anti-Xa level for 3.2% sodium citrate was 0.235 U/ml while the median level for 3.8% sodium citrate was 0.230 U/ml. We conclude that different sodium citrate concentrations give statistically equivalent anti-Xa levels for the same samples. This conclusion is in contrast to the findings of the effect of sodium citrate concentration on International Normalized Ratio (INR) and activated partial-thromboplastin time (aPTT). In accordance with previous recommendations, we advocate the exclusive use of 3.2% sodium citrate in an effort to standardize coagulation testing.

Anticoagulants↗

PubMed2002

Kinetic and biochemical analyses on the reaction mechanism of a bacterial ATP-citrate lyase.

The prokaryotic ATP-citrate lyase is considered to be a key enzyme of the carbon dioxide-fixing reductive tricarboxylic acid (RTCA) cycle. Kinetic examination of the ATP-citrate lyase from the green sulfur bacterium Chlorobium limicola (Cl-ACL), an alpha(4)beta(4) heteromeric enzyme, revealed that the enzyme displayed typical Michaelis-Menten kinetics toward ATP with an apparent K(m) value of 0.21 +/- 0.04 mm. However, strong negative cooperativity was observed with respect to citrate binding, with a Hill coefficient (n(H)) of 0.45. Although the dissociation constant of the first citrate molecule was 0.057 +/- 0.008 mm, binding of the first citrate molecule to the enzyme drastically decreased the affinity of the enzyme for the second molecule by a factor of 23. ADP was a competitive inhibitor of ATP with a K(i) value of 0.037 +/- 0.006 mm. Together with previous findings that the enzyme catalyzed the reaction only in the direction of citrate cleavage, these kinetic features indicated that Cl-ACL can regulate both the direction and carbon flux of the RTCA cycle in C. limicola. Furthermore, in order to gain insight on the reaction mechanism, we performed biochemical analyses of Cl-ACL. His273 of the alpha subunit was indicated to be the phosphorylated residue in the catalytic center, as both catalytic activity and phosphorylation of the enzyme by ATP were abolished in an H273A mutant enzyme. We found that phosphorylation of the subunit was reversible. Nucleotide preference for activity was in good accordance with the preference for phosphorylation of the enzyme. Although residues interacting with nucleotides in the succinyl-CoA synthetase from Escherichia coli were conserved in AclB, AclA alone could be phoshorylated with the same nucleotide specificity observed in the holoenzyme. However, AclB was necessary for enzyme activity and contributed to enhance phosphorylation and stabilization of AclA.

ATP Citrate (pro-S)-Lyase↗

PubMed2004

Regional citrate anticoagulation for continuous venovenous hemodiafiltration using calcium-containing dialysate.

BACKGROUND: Regional anticoagulation with trisodium citrate for continuous venovenous hemodiafiltration (CVVHDF) is an effective and safe alternative to heparin, especially in patients at high risk for bleeding. However, regional citrate anticoagulation is not used widely because current protocols are complex, labor intensive, and cumbersome. Existing protocols require the use of calcium-free dialysate with a continuous systemic calcium infusion to prevent hypocalcemia. We evaluated Anticoagulant Citrate Dextrose Formula A (ACD-A) solution for regional anticoagulation in CVVHDF in combination with a commercially available calcium-containing dialysis solution. METHODS: Thirty-eight patients in the intensive care units underwent citrate-based CVVHDF using low-calcium peritoneal dialysis solution (calcium, 5.0 mg/dL [1.25 mmol/L]). ACD-A infusion rate was adjusted to maintain postfilter ionized calcium (iCa++) levels at 1.0 to 2.0 mg/dL (0.25 to 0.5 mmol/L). Calcium chloride (10%) solution was administered intravenously every 6 hours on an as-needed basis to maintain systemic serum iCa++ levels at 3.5 to 4.0 mg/dL (0.88 to 1.0 mmol/L). RESULTS: CVVHDF was performed for a total of 394 days using 149 hemofilters. Mean hemofilter life span was 63.5 +/- 27.1 hours. Seventy-five percent, 61%, and 49% of hemofilters were patent at 24, 48, and 72 hours, respectively. No patient experienced a change in clinical status caused by hypocalcemia and/or signs and symptoms of citrate toxicity. Four patients developed metabolic alkalosis requiring 0.1 N of hydrochloric acid infusion. CONCLUSION: Our simplified technique of regional citrate anticoagulation for CVVHDF using calcium-containing dialysate is not associated with increased hemofilter clotting and obviates the need for a continuous systemic calcium infusion and calcium-free dialysate.

Adult↗

PubMed1995

Isotopomer analysis of citric acid cycle and gluconeogenesis in rat liver. Reversibility of isocitrate dehydrogenase and involvement of ATP-citrate lyase in gluconeogenesis.

We conducted an extensive mass isotopomer analysis of citric acid cycle and gluconeogenic metabolites isolated from livers of overnight fasted rats perfused with 4 mM glucose, 0.2 mM octanoate, 1 mM [U-13C3]lactate, and 0.2 mM [U-13C3]pyruvate, in the anterograde or retrograde mode. In both perfusion modes, two distinct isotopomer patterns were observed: (i) those of phosphoenolpyruvate, glucose, malate, and aspartate and (ii) those of citrate, alpha-ketoglutarate, glutamate, and glutamine. Key citric acid cycle parameters and, hence, rates of gluconeogenesis, calculated (Lee, W.-N.P. (1989) J. Biol. Chem. 264, 13002-13004 and Lee, W.-N.P. (1993) J. Biol. Chem. 268, 25522-25526) from our mass isotopomer data did not only vary, but lead to conclusions inconsistent with Lee's citric acid cycle model. Compared to lactate and pyruvate uptake, which sets an upper limit to glucose production, rates of gluconeogenesis calculated (i) with the phosphoenolpyruvate and citrate data were similar, but those calculated (ii) with the glutamate data amounted to only 60%, which is unlikely. All these conclusions are independent of the perfusion modes. We provide evidence that the following processes contribute to the observed labeling discrepancy: (i) the reversibility of the isocitrate dehydrogenase reaction and (ii) an active citrate cleavage pathway for the transfer of the oxaloacetate carbon skeleton from mitochondria to the cytosol. Also, a good fit of our labeling data was obtained with a model of citric acid cycle and gluconeogenesis which we developed to incorporate the above reactions (Fernandez, C.A., and Des Rosiers, C. (1995) J. Biol. Chem. 270, 10037-10042). The following conclusions can be drawn from the calculated reaction rates: (i) about half of the lactate conversion to glucose occurs via the citrate cleavage pathway, (ii) the flux through the reversal of the isocitrate dehydrogenase reaction is almost as fast as that through the citrate synthase reaction, and (iii) the flux through citrate synthase and alpha-ketoglutarate dehydrogenase is 1.6- and 3.2-fold that through pyruvate carboxylase, respectively.

ATP Citrate (pro-S)-Lyase↗

PubMed1997

Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing.

The effects of 3.2% and 3.8% sodium citrate concentration on the results of routine coagulation assays (prothrombin time [PT] and activated partial thromboplastin time [aPTT]) were evaluated by means of two sets of reagents, one responsive and the other nonresponsive. Five groups were entered in the study: healthy volunteers; outpatients receiving stable oral anticoagulant therapy; and hospitalized patients receiving intravenous (i.v.) heparin therapy, both i.v. heparin and oral anticoagulant therapy, or no anticoagulant therapy. With use of nonresponsive PT and aPTT reagents, varying the citrate concentration has little clinical significance except in patients receiving i.v. heparin therapy. In contrast, when responsive PT and aPTT reagents are used, the concentration of sodium citrate anticoagulant has a significant effect on assay results. Eighteen percent of samples from patients receiving stable oral anticoagulant therapy demonstrated a change of less than 0.7 INR (International Normalized Ratio) units between citrate concentrations. Nineteen percent of patients receiving i.v. heparin therapy had a greater than 7-second difference when aPTT results were compared. These data demonstrate that citrate concentration affects the results of coagulation tests. On the basis of these data, it is recommended that 3.2% citrate be used for all coagulation tests.

Anticoagulants↗

PubMed2000

The effect of sodium citrate in arterial catheters on acid-base and electrolyte measurements.

OBJECTIVE: To compare the effects of heparin or sodium citrate used to anticoagulate indwelling arterial catheters on acid-base and electrolyte measurements. DESIGN: Randomized controlled trial. SETTING: Medical-surgical university-affiliated intensive care unit. SUBJECTS: Twenty patients with indwelling arterial catheters. INTERVENTIONS: Patients were randomly allocated to have ten 1-mL aliquots of blood sampled serially from an arterial catheter maintained with either heparin or sodium citrate. A sample then obtained by arterial puncture provided true measurement values. Acid-base and electrolyte measurements of whole blood were obtained from each sample by means of a Coming 860 analyzer. MEASUREMENTS AND MAIN RESULTS: Contamination with sodium citrate lowered ionized calcium and pH but increased glucose and Pco2. Heparin produced negligible effects on those measurements. When sodium citrate was used, reliable measurements were not obtained for ionized calcium, pH, and glucose, even after 9 mL of blood had been discarded. However, reliable P(CO2) measurements were obtained after 2 mL of blood was discarded. CONCLUSIONS: Sodium citrate used to maintain arterial catheters can contaminate blood samples. The result of that contamination can mimic severe hypocalcemia, metabolic acidosis, and mild hyperglycemia. Failure to recognize the effects of sodium citrate on acid-base and electrolyte measurements may lead to changes in treatment that could affect patient outcome adversely.

Acid-Base Equilibrium↗

PubMed1980

Regional and subcellular distribution of ATP-citrate lyase and other enzymes of acetyl-CoA metabolism in rat brain.

The activities of ATP-citrate lyase in frog, guinea pig, mouse, rat, and human brain vary from 18 to 30 mu mol/h/g of tissue, being several times higher than choline acetyltransferase activity. Activities of pyruvate dehydrogenase and acetyl coenzyme A synthetase in rat brain are 206 and 18.4 mu mol/h/g of tissue, respectively. Over 70% of the activities of both choline acetyltransferase and ATP-citrate lyase in secondary fractions are found in synaptosomes. Their preferential localization in synaptosomes and synaptoplasm is supported by RSA values above 2. Acetyl CoA synthetase activity is located mainly in whole brain mitochondria (RSA, 2.33) and its activity in synaptoplasm is low (RSA, 0.25). The activities of pyruvate dehydrogenase, citrate synthase, and carnitine acetyltransferase are present mainly in fractions C and Bp. No pyruvate dehydrogenase activity is found in synaptoplasm. Striatum, cerebral cortex, and cerebellum contain similar activities of pyruvate dehydrogenase, citrate synthase, carnitine acetyltransferase, fatty acid synthetase, and acetyl-CoA hydrolase. Activities of acetyl CoA synthetase, choline acetyltransferase and ATP-citrate lyase in cerebellum are about 10 and 4 times lower, respectively, than in other parts of the brain. These data indicate preferential localization of ATP-citrate lyase in cholinergic nerve endings, and indicate that this enzyme is not a rate limiting step in the synthesis of the acetyl moiety of ACh in brain.

ATP Citrate (pro-S)-Lyase↗

PubMed1986

Apparent inhibition of ATP citrate lyase by L-glutamate in vitro is due to the presence of glutamine synthetase.

Preincubation in assay mixture for 30 min at 37 degrees C of ATP citrate lyase from rat brain and liver results in 65-70% inhibition in the presence of 10 mM L-glutamate. This inhibition is specific since none of the known brain metabolites of glutamate shows this effect. ATP and ammonium sulphate-suspended, commercially purified malate dehydrogenase are both important in the generation of inhibition; citrate and NADH are not. The ATP citrate lyase activity in desalted crude extracts and 11% polyethylene glycol-precipitated fractions is inhibited but the enzyme purified by dye affinity chromatography is unaffected. Such purification reveals the presence of a factor responsible for the generation of the inhibition shown to be of Mr 380,000. These lines of evidence implicate endogenous glutamine synthetase, and the involvement of this enzyme is established by the use of its inhibitor L-methionine sulphoximine and by the addition of purified glutamine synthetase to restore the glutamate inhibition of purified ATP citrate lyase. The phenomenon probably arises from the production by glutamine synthetase of ADP, a known product inhibitor of ATP citrate lyase. Therefore contrary to previous reports elsewhere, L-glutamate has no role in the regulation of brain ATP citrate lyase and thus the supply of cytoplasmic acetyl groups for biosynthesis.

ATP Citrate (pro-S)-Lyase↗

PubMed2005

Regional citrate versus systemic heparin anticoagulation for continuous renal replacement in critically ill patients.

BACKGROUND: We determined the effect of regional citrate versus systemic heparin anticoagulation for continuous renal replacement therapy in critically ill subjects suffering from acute renal failure who were not at high risk for hemorrhagic complications. METHODS: Between April 1999 and June 2002, 30 critically ill subjects requiring continuous renal replacement therapy and using 79 hemofilters were randomly assigned to receive regional citrate or systemic heparin anticoagulation. RESULTS: The median hemofilter survival time was 124.5 hours (95% CI 95.3 to 157.4) in the citrate group, which was significantly longer than the 38.3 hours (95% CI 24.8 to 61.9) in the heparin group (P < 0.001). Increasing illness severity score, male gender, and decreasing antithrombin-III levels were independent predictors of an increased relative hazard of hemofilter failure. After adjustment for illness severity, antithrombin-III levels increased significantly more over the period of study in the citrate as compared to the heparin group (P= 0.038). Moreover, after adjustment for antithrombin-III levels and illness severity score, the relative risk of hemorrhage with citrate anticoagulation was significantly lower than that with heparin (relative risk of 0.14; 95% CI 0.02 to 0.96, P= 0.05). CONCLUSION: Compared with systemic heparin anticoagulation, regional citrate anticoagulation significantly increases hemofilter survival time, and significantly decreases bleeding risk in critically ill patients suffering from acute renal failure and requiring continuous renal replacement therapy.

Acute Kidney Injury↗

PubMed2003

Effects of sodium citrate ingestion before exercise on endurance performance in well trained college runners.

OBJECTIVE: To test the hypothesis that sodium citrate administered two hours before exercise improves performance in a 5 km running time trial. METHODS: A total of 17 male well trained college runners (mean (SD) O(2)MAX 61.3 (4.9) ml/kg/min) performed a 5 km treadmill run with and without sodium citrate ingestion in a random, double blind, crossover design. In the citrate trial, subjects consumed 1 litre of solution containing 0.5 g of sodium citrate/kg body mass two hours before the run. In the placebo trial, the same amount of flavoured mineral water was consumed. RESULTS: The time required to complete the run was faster in the citrate trial than the placebo trial (1153.2 (74.1) and 1183.8 (91.4) seconds respectively; p = 0.01). Lower packed cell volume and haemoglobin levels were found in venous blood samples taken before and after the run in the citrate compared with the placebo trial. Lactate concentration in the blood sample taken after the run was higher in the citrate than the placebo trial (11.9 (3.0) v 9.8 (2.8) mmol/l; p<0.001), and glucose concentration was lower (8.3 (1.9) v 8.8 (1.7) mmol/l; p = 0.02). CONCLUSION: The ingestion of 0.5 g of sodium citrate/kg body mass shortly before a 5 km running time trial improves performance in well trained college runners.

Adult↗

PubMed2001

Effects of sodium citrate, low molecular weight heparin, and prostaglandin E1 on aggregation, fibrinogen binding, and enumeration of equine platelets.

OBJECTIVE: To investigate the effects of sodium citrate, low molecular weight heparin (LMWH), and prostaglandin E1 (PGE1) on aggregation, fibrinogen binding, and enumeration of equine platelets. SAMPLE POPULATION: Blood samples obtained from 4 Thoroughbreds. PROCEDURE: Blood was collected into syringes in the ratio of 9 parts blood:1 part anticoagulant. Anticoagulants used were sodium citrate, LMWH, sodium citrate and LMWH, or 300 nM PGE1/ml of anticoagulant. Platelet aggregation in response to ADP, collagen, and PGE1 was assessed, using optical aggregometry. Platelet activation was evaluated, using flow cytometry, to detect binding of fluorescein-conjugated anti-human fibrinogen antibody. Plasma concentration of ionized calcium was measured, using an ion-selective electrode. RESULTS: Number of platelets (mean +/- SEM) in samples containing LMWH (109.5+/-11.3 x 10(3) cells/microl) was significantly less than the number in samples containing sodium citrate (187.3+/-30.3 x 10(3) cells/microl). Increasing concentrations of sodium citrate resulted in reductions in platelet aggregation and plasma concentration of ionized calcium. Addition of PGE1 prior to addition of an agonist inhibited platelet aggregation in a concentration-dependent manner, whereas addition of PGE1 4 minutes after addition of ADP resulted in partial reversal of aggregation and fibrinogen binding. CONCLUSIONS AND CLINICAL RELEVANCE: A high concentration of sodium citrate in blood samples decreases plasma concentration of ionized calcium, resulting in reduced platelet aggregation and fibrinogen binding. Platelets tend to clump in samples collected into LMWH, precluding its use as an anticoagulant. Platelet aggregation and fibrinogen binding can be reversed by PGE1, which may result in underestimation of platelet activation.

Adenosine Diphosphate↗