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At least 19 recordsLinked to original sources
PubMed1990

Effect of ascorbic acid, sodium citrate, sodium bicarbonate, and their combination effect on the binding of 59Fe2+ and 59Fe3+ to plasma membrane of lactating mouse mammary gland.

Isolated plasma membranes of lactating mouse mammary gland were treated with different concentrations of ascorbate, sodium citrate, sodium bicarbonate, and combinations of them (from 16 x 10(-10) to 4 x 10(-6) moles/L) and studied for the binding of 59Fe2+ and 59Fe3+ at pH 7.4. The results show that the Fe3+ form of iron is under a greater influence of anions used in these experiments. The Fe2+ form of iron is weakly bounded and affected. It is suggested that the form with a greater positive electric charge is more effectively bound to the receptors in plasma membranes.

Animals↗
PubMed1998

Influence of ascorbic acid, sodium citrate, and sodium bicarbonate on the uptake of 59Fe-transferrin, 54Mn-transferrin, and 65Zn-transferrin from lactating mouse mammary gland cells.

The effects of ascorbic acid, sodium citrate, and sodium bicarbonate on 59Fe-transferrin, 54Mn-transferrin, and 65Zn-transferrin uptake by the receptors disposed of plasma membrane isolated from lactating mouse mammary gland cells have been investigated. The effect of 10(-2) mol/L ascorbic acid alone and in combination with NaHCO3 on the 59Fe-transferrin uptake is significant and positive. 54Mn-transferrin and 65Zn-transferrin binding to the cell receptors are influenced optimally by 0.5 mol/L sodium bicarbonate. Sodium citrate alone or in combination with other substances always has a negative effect on binding of these three metals. It is suggested that a precise mechanism may exist with large possibilities to rearrange metal uptake and its transport from blood to milk.

Animals↗
PubMed1990

Aspiration pneumonitis prophylaxis in obstetric anaesthesia: comparison of effervescent cimetidine-sodium citrate mixture and sodium citrate.

One hundred and forty-seven patients undergoing elective or emergency Caesarean section under general anaesthesia were allocated randomly to three groups: group 1 (n = 28) received no premedication; group 2 (n = 58) received 0.3-molar sodium citrate 15 ml (sodium citrate 1.16 g); group 3 (n = 61) received effervescent cimetidine-sodium citrate combination (cimetidine 400 mg with sodium citrate 0.9 g) after entering the operating room. Gastric pH was measured at tracheal intubation (pH1) and extubation (pH2). Mean pH1 and mean pH2 values in group 1 were, respectively, 2.25 (SD 1.35) and 2.83 (1.64). Mean pH1 and pH2 values in group 2 were, respectively, 4.38 (1.44) and 4.57 (1.51). In group 3 mean pH1 and pH2 values were, respectively, 5.07 (1.13) and 5.37 (1.30). Percentages of patients with pH1 less than or equal to 2.5 in groups 1, 2 and 3 were, respectively, 75, 13.8 and 1.6. Percentages of patients with pH2 less than or equal to 2.5 in groups 1, 2 and 3 were 50, 10.3 and 1.6, respectively.

Adult↗
PubMed1983

Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts.

Effects of potassium citrate therapy (60 mEq/day) on urinary chemistries and crystallization were compared to those of sodium citrate treatment in five patients with uric acid lithiasis. Both alkali treatments significantly increased urinary pH (P less than 0.001), from 5.35 +/- 0.18 SD to 6.68 +/- 0.14 for potassium citrate and 6.73 +/- 0.20 for sodium citrate. During potassium citrate therapy, urinary calcium significantly declined from 154 +/- 47 mg/day to 99 +/- 23 mg/day (P less than 0.01) and urinary citrate rose from 398 +/- 119 mg/day to 856 +/- 103 mg/day (P less than 0.001). The urinary saturation (activity product ratio) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation (P less than 0.01), and the inhibitor activity against calcium oxalate precipitation (formation product ratio) significantly increased. However, sodium citrate therapy did not significantly decrease urinary calcium (to 139 +/- 24 mg/day), although it increased urinary citrate substantially (to 799 +/- 89 mg/day, P less than 0.01). Urinary environment became supersaturated with respect to brushite (calcium phosphate) and monosodium urate. The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group; in two patients, it decreased by more than 30%. The results indicate that (1) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH, and (2) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones, whereas sodium citrate may not.

Adult↗
PubMed1999

The effect of citric acid, lactic acid, sodium citrate and sodium lactate, alone and in combination with nisin, on the growth of Arcobacter butzleri.

The importance of Arcobacter spp. as a cause of human foodborne illness is unresolved. Organic acids and their sodium salts, and nisin are preservatives commonly used in the type of foods from which the organism is recovered. In this study their effect on the growth of A. butzleri in culture, alone and in combination, was investigated. At 0.5%, 1.0% and 2.0% lactic and citric acids inhibited A. butzleri growth; 2% sodium lactate was effective in inhibiting growth over 8 h incubation but not over longer periods. Sodium citrate was more effective than sodium lactate. Nisin alone inhibited A. butzleri growth at 500 IU ml-1 over 5 h. It did not enhance the effect of sodium citrate inhibition but it did augment the effect of sodium lactate alone over 8 h.

Arcobacter↗
PubMed1992

A comparison of sodium citrate and sodium citrate/ranitidine combination for acid aspiration prophylaxis.

The effectiveness of sodium citrate and sodium citrate/ranitidine were compared in two randomised groups of elective caesarean patients during the various phases of anaesthesia. The mean pH values (3.5, 3.3, 3.6) were lower in the citrate group compared to the citrate/ranitidine group (6.1, 6.3, 5.9). The percentage of patients with pH values less than 2.5 was 40% in the citrate group compared to 7% in the citrate/ranitidine group. Sodium citrate alone is less effective than sodium citrate/ranitidine for acid aspiration prophylaxis.

Adolescent↗
PubMed1984

Oral rehydration therapy: efficacy of sodium citrate equals to sodium bicarbonate for correction of acidosis in diarrhoea.

Forty patients with moderate degrees of dehydration and acidosis because of acute watery diarrhoea were successfully treated randomly with either WHO recommended oral rehydration solution containing 2.5 g sodium bicarbonate or an oral solution containing 2.94 g sodium citrate in place of sodium bicarbonate per litre of oral rehydration rehydration solution. Efficacies were compared by measuring oral fluid intake, stool and vomitus output, change in body weight, hydration status, and rate of correction of acidosis during a period of 48 hours. Seventy five per cent (21 cases) in the citrate group and 83% (19 cases) in the bicarbonate group were successfully rehydrated (p greater than 0.05). There were no significant differences in intake, output, gain in body weight, fall in haematocrit and plasma specific gravity, and correction of acidosis between the two groups of patients within 48 hours after initiation of therapy. The solution with sodium citrate base was as effective as WHO-oral rehydration solution for management of diarrhoea. This study shows the efficacy, safety, and acceptability of citrate containing oral rehydration solution for rehydration and correction of acidosis in diarrhoea.

Acidosis↗
PubMed1984

The effect of metoclopramide on gastric contents after preoperative ingestion of sodium citrate.

Because sodium citrate is known to increase both gastric pH and gastric volume while metoclopramide decreases gastric volume, we evaluated, in a double-blind randomized study, the effect of combining metoclopramide with sodium citrate on gastric pH and volume after induction of anesthesia in 60 female patients to determine whether gastric pH could be increased at the same time that gastric volume was decreased. All patients received 50-ml sodium citrate. To mimic standard anesthetic practice, all patients were premedicated: 20 patients received meperidine alone, 20 received meperidine plus 20-mg metoclopramide, and 20 received diazepam plus 20-mg metoclopramide. Metoclopramide failed to decrease median gastric volume or to increase the number of patients with gastric volumes less than 25 ml. There was no difference in median pH values in the three groups of patients. In patients receiving metoclopramide, the risk of pH values less than 2.5 was greater with gastric volumes less than 25 ml than in patients with volumes greater than or equal to 25 ml. We conclude that preoperative metoclopramide does not decrease gastric volume in patients premedicated with meperidine or diazepam and that when gastric volume was less than 25 ml the neutralizing effect of sodium citrate was lost.

Adult↗
PubMed1978

Antacid properties of a sodium citrate preparation.

A sodium citrate preparation (Citro-Soda; Abbott) given in single doses of 4 or 12 g, satisfactorily increased the pH level of urine without affecting the systemic acid-base balance. When the sodium citrate preparation was administered in the 12-g single dose the gastric pH level was raised above 3,0 in a significant number of subjects. Similar results were obtained with both single doses (4 and 12 g) after 3 - 6 days of continuous therapy at the appropriate dose given every 6 hours. It is concluded that the urine-alkalinizing sodium citrate preparation reduced intragastric acidity significantly.

Adult↗
PubMed1988

Alkali action on the urinary crystallization of calcium salts: contrasting responses to sodium citrate and potassium citrate.

Alkali therapy is used commonly to prevent recurrent stone formation in patients with distal renal tubular acidosis. We compared the effects of potassium citrate to those of sodium citrate in 6 well defined cases of incomplete distal renal tubular acidosis. The patients were studied during a control phase, during potassium citrate treatment (80 mEq. per day) and during sodium citrate treatment (80 mEq. per day) chosen in random order. Potassium citrate caused a decrease in urinary calcium and a significant increase in urinary citrate that resulted in a significant decrease in the urinary saturation of calcium oxalate. It did not alter the saturation of brushite and sodium urate. However, while sodium citrate also was able to increase the urinary citrate level, there was no decrease in the urinary calcium (owing to the increased sodium load). Thus, the urinary saturation of calcium oxalate did not decrease as much as with potassium citrate and the saturation of brushite increased significantly. Moreover, the urinary saturation of sodium urate increased significantly owing to the enhanced sodium excretion. The results suggest that potassium citrate therapy may retard the crystallization of calcium oxalate and may not cause calcium phosphate crystallization. In contrast, sodium citrate may have no effect or it sometimes may accentuate the crystallization of calcium salts. Thus, our study supports the potential clinical advantage of potassium citrate therapy over sodium alkali treatment in patients with incomplete distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗
PubMed2003

Effect of sodium citrate on structure-function relationships of Cheddar cheese.

The objective of this study was to determine the effect of sodium citrate on the structure and functionality of Cheddar cheese. The hypothesis was that citrate (sodium citrate) injection would affect cheese properties mainly through its effect on bound calcium (calculated as the difference between total calcium and the water-soluble calcium content of a cheese extract). A 9-kg block of Cheddar cheese was made, vacuum-packaged, and then stored for 2 wk at 4 degrees C. After storage, the cheese was cut into 0.5- to 0.6-kg blocks that were vacuum-packaged and stored for 1 wk at 4 degrees C prior to injection. Cheese blocks were then high-pressure injected with a buffer solution (pH 5.27) containing 40% (wt/ wt) citric acid trisodium dihydrate and 6.25% (wt/wt) anhydrous citric acid, from zero (control) to five times (successive injections performed 24 h apart). Increased citric acid content of cheese from 0.22 (uninjected) to 1.39% (after five injections) caused phosphate solubilization. Thus, the calculated bound phosphate content of cheese decreased from 0.54 to 0.45 mmol/g of protein. However, unexpectedly, the soluble calcium content decreased from 0.34 (control) to 0.28 mmol/g of protein (after five injections), whereas the bound calcium content remained unchanged (0.42 mmol/g of protein). The decrease in soluble calcium probably resulted from the formation and concentration of crystals in the cheese surface, which was not included in samples for analysis, and from the expulsion of serum from within the cheese. Higher concentration of solutes in the water phase of cheese would increase the volume of serum, but the cheese had limited holding capacity and serum was expelled. Citrate injection increased the sodium content of cheese from 0.63 to 0.93%, but it had no effect on cheese pH (5.2). After five injections, the protein matrix expanded, occupying an increased area of cheese matrix (83 vs. 78%). Even though citrate injection had no effect on bound calcium, and thus the rate and extent of cheese flow were unaffected, increased phosphate solubilization, and possibly decreased ionic calcium content, resulted in expansion of the protein matrix and increased cheese hardness.

Calcium↗
PubMed1985

The effect of sodium citrate on the stimulation of polymorphonuclear leukocytes.

Topical administration of sodium citrate reduces the incidence of corneal ulceration and perforation following an alkali burn to the eye. The specific mechanism by which sodium citrate prevents the ulceration is not understood, although citrate does inhibit the infiltration of polymorphonuclear leukocytes (PMNs) into the cornea following an alkali burn. In the present study, the effects of sodium citrate and another calcium chelator, ethylene glycol bis (beta-aminoethylether)-N,N'tetraacetic acid (EGTA), upon PMN oxygen consumption and lysosomal enzyme release were determined. Oxygen consumption was measured polarographically using a Clark-type oxygen electrode, and lysosomal enzyme release was determined by intra- and extra-cellular measurements of myeloperoxidase activity. Opsonized zymosan and N-formylmethionylleucylphenylalanine (FMLP) were used to stimulate neutrophil oxygen consumption and lysosomal release. Both sodium citrate and EGTA inhibited PMN oxygen consumption and lysosomal enzyme release in response to opsonized zymosan. In contrast, neither sodium citrate nor EGTA reduced PMN oxygen consumption or lysosomal enzyme release in response to FMLP. Therefore, the ability of sodium citrate (and EGTA) to inhibit PMN stimulation is dependent upon the choice of stimulus. Until the inflammatory mediators involved in the ulcerative process following an alkali burn to the eye are delineated, the impact of sodium citrate upon PMN stimulation in vivo cannot be resolved.

Burns, Chemical↗