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PubMed1989

Urine citrate and renal stone disease.

Calcium stone disease is attributable to supersaturation of the urine with calcium and other salts, the presence of substances that promote crystallization and a deficiency of inhibitors of crystallization. Citrate is a potent inhibitor of calcium oxalate and calcium phosphate stone formation whose excretion is diminished in some patients with stone disease owing to idiopathic causes or secondary factors such as bowel disease and use of thiazides. The pH within the proximal tubule cells is an important determinant of citrate excretion. Multivariate analysis has shown that the urine concentrations of calcium and citrate are the most important factors in stone formation. In uncontrolled studies potassium citrate, which increases urinary citrate excretion, appears to be promising as a therapeutic agent for patients with stone disease and hypocitraturia refractory to other treatment. On the other hand, there are potential drawbacks to sodium alkali therapy, such as the precipitation of calcium phosphates.

Citrates↗

PubMed1989

Efficacy of zinc citrate ascorbate for treatment of canine cataracts.

Efficacy of zinc citrate ascorbate was evaluated in 146 dogs (265 eyes) that had various lens opacities. Zinc citrate ascorbate or saline placebo drops were applied topically once or twice daily for 4 to 31 weeks. Of 138 eyes treated with zinc citrate ascorbate, 86 eyes (62.3%) had no change, 48 eyes (34.8%) had increased lens opacity, and 4 eyes (2.9%) had decreased lens opacity. Of 127 eyes treated with a saline placebo, 99 eyes (77.9%) had no change, 25 eyes (19.7%) had increased lens opacity, and 3 eyes (2.4%) had decreased lens opacity. Zinc citrate ascorbate drops were not significantly (P = less than 0.05) more effective in clearing cataracts than were saline drops. Seemingly, zinc citrate ascorbate drops may have caused lens opacities to increase in area and density.

Animals↗

PubMed1989

Studies on citrate metabolism in normal subjects and kidney stone patients.

The study was carried out in order to investigate citrate metabolism (i.e. serum levels, filtered load, tubular reabsorption, total and fasting urinary excretion) in a large group of normal subjects (n = 39) and kidney stone patients (n = 45). We found that mean serum citrate levels and filtered loads were similar in the two groups studied. On the other hand, both the 24-hour urinary citrate and the fasting citrate/creatinine ratio were significantly reduced, whereas the mean tubular reabsorption of citrate appeared to be significantly increased in kidney stone patients in respect to control subjects. A good correlation was found between the fasting and the 24-hour citrate/creatinine ratio in both normal subjects (r = 0.84, p less than 0.001) and kidney stone patients (r = 0.89, p less than 0.001). Our data indicate that the kidney appears to be involved in the pathogenesis of hypocitraturia in kidney stone patients and that a substantial proportion of these patients show a reduced urinary excretion of citrate. Finally, the evaluation of the fasting citrate/creatinine ratio may replace the measurement of the substance on the basis of a 24-hour urine collection.

Adolescent↗

PubMed1988

The effects of citrate on the adherence of neutrophils to nylon fibers in vitro.

The therapeutic effect of citrate on alkali-burned eyes is thought to be the result of inhibition of PMN activities while ascorbate apparently stimulates the production of new collagen by scorbutic fibroblasts. Attachment of PMNs to the vascular endothelium is the initial PMN response to mediators and must occur before diapedesis and chemotaxis can produce a tissue infiltrate. The present study was undertaken to test the effects of citrate or ascorbate on the in vitro adherence of resting and leukotriene B4 (LTB4)-treated PMNs. Citrate preincubation of resting or LTB4-treated PMNs inhibited adherence in a dose-dependent manner. Inhibition of LTB4 augmented adherence by 12 mM citrate was effectively reversed by the addition of Ca2+ and Mg2+ (6 mM each). Ascorbate had no significant effect on the adherence of resting or LTB4 treated PMNs. In addition we wished to test the effectiveness of the breakdown product(s) from alkali burned collagen (Type 1) as an augmentor of adherence because of its effectiveness as a locomotory and respiratory burst stimulant. These break-down product(s) had no effect on the adherence of resting or LTB4-treated PMNs unless bovine serum albumin (BSA) was omitted from the incubation mixture. In the absence of BSA, these breakdown products inhibited both types of adherence in a dose-dependent manner with dilutions from 1:10 to 1:1000. This inhibition is probably not clinically meaningful since PMN adherence takes place in the vasculature where BSA would always be present. As a consequence of citrate inhibition of adherence in vivo, PMNs would be denied access to the injury site, trapping them in a resting state within the circulatory system.

Ascorbic Acid↗

PubMed1989

[Intraoperative, direct and continuous measurement of stomach pH following pretreatment with ranitidine or sodium citrate].

We carried out continuous direct pH measurements of gastric fluid in 49 female patients pretreated with 300 mg ranitidine by mouth on the evening prior to surgery and 150 mg by mouth before the operation. A further 51 women were pretreated with 30 ml sodium citrate shortly before admission to the operating room. Twenty patients received 30 ml sodium citrate via a separate gastric tube after the first pH measurement; 22 were given no premedication. In 95% of cases, 30 ml sodium citrate was found to increase the pH to over 3.5 within 5 min; a failure rate of 5% can therefore be expected. This can be explained mainly by the failure of sodium citrate to mix thoroughly with the gastric fluid. Pretreatment with ranitidine increased the pH to over 4.0 in every case, and the pH on extubation was still over 4.0 even after delayed pH on extubation was still over 4.0 even after delayed or prolonged operations. We recommend that 30 ml sodium citrate be given shortly before the beginning of emergency obstetric operations. However, we prefer ranitidine for elective operations in patients at risk for aspiration because it increases of the gastric fluid pH to at least 4.0 in every case.

Citrates↗

PubMed1988

[Citrate (CG-120) therapy for urolithiasis. 1. Clinical effects].

Urinary citrate is an important determinant for crystallization of calcium salts, and recently oral administration of citrate has been suggested to be clinically useful in the management of renal stone disease. The effect of CG-120, a citrate compound (potassium citrate, sodium citrate and citric acid) produced by Dr. Madaus (Germany), on upper urinary tract stones was investigated in 398 patients in this study group. The patients were treated with 3 or 4 g CG-120 daily. Two hundred thirty-one of them were treated accurately according to the protocol of the study for more than 32 weeks. The cumulative percentage of positive clinical effect for the stone (disappearance, passage or decrease in size) was 30.3% (70/231). There were no differences in the clinical effect between the group of 3 g/day and the group of 4 g/day. CG-120 seemed to be more effective in the cases of ureteral stone, young patients and females, but was less effective in the recurrent stone formers. Although there were 45 episodes of side effects in 38 patients in this study, no serious side effects attributed to CG-120 were experienced. CG-120 was proved as a useful drug in the treatment of upper urinary tract calculi as well as its prevention.

Adolescent↗

PubMed1978

Effect of shear rate on platelet interaction with subendothelium in citrated and native blood. I. Shear rate--dependent decrease of adhesion in von Willebrand's disease and the Bernard-Soulier syndrome.

Previous studies have demonstrated impaired adhesion of platelets to the subendothelium in von Willebrand's disease. These studies were performed by circulating (in a closed system) citrated whole blood through a chamber containing everted segments of rabbit aorta from which the endothelium had been removed by balloon catheter. The average wall shear rate was 800 sec-1, and the perfusion time was 10 min. In the present study we measured the interaction of platelets with subendothelium in native (nonanticoagulated) blood, using a recently described technique in which the vessel segments are perfused with directly sampled venous blood. The system was open; that is, the blood was not recirculated. We used blood flow rates of 20, 40, and 50 ml/min, which correspond to calculated shear rates of 1300, 2600, and 3300 sec-1 and perfusion times of 3, 2, and 2 min, respectively. For comparison, parallel studies at 1300 sec-1 were also obtained with citrated blood. In normal subjects, at a shear rate of 1300 sec-1, platelet adhesion was less in native blood than in citrated blood, but thrombus formation was greater. Platelet adhesion in five patients with von Willebrand's disease was decreased in both citrated and native blood. The magnitude of the adhesion defect was strongly dependent on the shear rate. Thus, in citrated blood studied at a shear rate of 1300 sec-1, adhesion was 75% less than in normal subjects, whereas in previous studies at 800 sec-1 the reduction in adhesion was 29%. In native blood, adhesion in von Willebrand's disease was normal at a shear rate of 1300 sec-1, whereas 53% and 77% reductions in adhesion were obtained at shear rates of 2600 and 3300 sec-1, respectively. The latter shear rates studied, adhesion of platelets in native blood was also decreased in the Bernard-Soulier syndrome but was normal in hemophilia and afibrinogenemia. Our findings with native blood provide further evidence that impaired adhesion of platelets to the vessel wall accounts for the hemostatic defect in von Willebrand's disease. In addition, this adhesion defect is shear rate-dependent.

Adolescent↗

PubMed1987

Isoproterenol and insulin control the cellular localization of ATP citrate-lyase through its phosphorylation in adipocytes.

The enzyme ATP citrate-lyase of the fatty acid synthesis pathway is phosphorylated in vitro and in isolated cells. However, no effect of phosphorylation on the enzyme activity has been detected. It is demonstrated that the beta-adrenergic agonist isoproterenol or insulin both promote an immobilization of ATP citrate-lyase, detected in digitonin-permeabilized adipocytes. This effect was reproduced by the cyclic AMP analog cyclic 8-bromo-AMP. The beta-adrenergic antagonist propranolol blocked, but failed to reverse, the isoproterenol-directed effect. Propranolol also failed to reverse the isoproterenol-induced increased phosphorylation of ATP citrate-lyase specifically. In response to increasing concentrations of isoproterenol, an increased extent of phosphorylation of ATP citrate-lyase was paralleled by an increased immobilization of the enzyme. It is suggested that the state of phosphorylation of ATP citrate-lyase in adipocytes controls the localization in the cell.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1979

In vitro citrate synthesis by the dog kidney. Investigations with cortex, red and white medulla slices.

In vitro utilization or production of citrate by the cortex, outer medulla or inner medulla of dog kidney was measured. Our data show: 1. An in vitro citrate synthesis or utilization capacity of the cortex greater than that of the red medulla. 2. An effect of pH on citrate synthesis or utilization capacity of the cortex, an effect not seen with medullary slices. 3. An absence of citrate synthesis or utilization by white medulla slices. It would seem that the citrate found in the white medulla and the papilla of the dog kidney in vivo was not produced in situ.

Animals↗

PubMed1981

Compatibility of lithium citrate syrup with 10 neuroleptic solutions.

The visual compatibility of lithium citrate syrup (1.6 meq Li+/ml) in mixtures with each of 10 neuroleptic drug solutions or concentrates was studied. Lithium citrate syrup (5 or 10 ml) was mixed with four volumes (representing minimal to maximal clinical dosages) of each of 10 liquid neuroleptic drug products--chlorpromazine hydrochloride, haloperidol lactate, thioridazine hydrochloride, trifluoperazine hydrochloride, fluphenazine hydrochloride, loxapine hydrochloride, mesoridazine besylate, molindone hydrochloride, perphenazine, and thiothixene hydrochloride. Samples were prepared in duplicate by both orders of mixing at 25 +/- 2 degrees C and 4 +/- 1 degrees C and observed visually immediately and six hours later. Samples observed to be incompatible were centrifuged, and resulting layers were tested for drug with thin-layer chromatography. At six hours after mixing, pH values of the mixtures were measured. Chlorpromazine, haloperidol, thioridazine, and trifluoperazine products were incompatible with lithium citrate syrup; other products were compatible. Centrifugation of incompatible mixtures yielded two liquid phases--a more voluminous clear supernatant and a viscous, translucent, hydrophobic sediment. Thin-layer chromatography verified the presence of the neuroleptic drug in both phases. The incompatibility is independent of pH and lithium or citrate ions. The four incompatible neuroleptic solutions were each mixed with 1.64 M sodium chloride solution, and the same incompatibility was noted as with 5 ml of lithium citrate syrup. This suggested that the precipitation is caused by excessive ionic strength in the mixtures, resulting in salting out of undissociated, solvated ion pairs of the protonated neuroleptic bases and their respective anions. The incompatible mixtures should be avoided because clinically important underdoses could occur.

Antipsychotic Agents↗

PubMed1982

Inhibition of soluble guanylate cyclase activity by citrate.

Soluble guanylate cyclase activity from guinea pig heart is inhibited by increasing concentrations of sodium citrate. The Ki value was found to be 2.83 +/- 0.05 mM in the presence of 3 mM Mn2+ and 0.6 mM GTP. Citrate acts by lowering Vmax and increasing the apparent values of Km for GTP and K0.5 for Mn2+ and Mg2+. The soluble guanylate cyclase, activated by sodium nitroprusside, was also inhibited by citrate. This inhibitory action of citrate was not restricted to soluble guanylate cyclase activity of the heart and has been demonstrated also in the supernatant of lung, liver, diencephalon and in the homogenate of blood platelets. Since citrate is known to be an important intermediate of metabolism, its intracellular concentration may be also of relevance for guanylate cyclase activity.

Animals↗

PubMed1984

A kit for citrate in foodstuffs adapted for assay of serum and urine.

A kit method for rapid analysis of citrate in foodstuffs, based on use of citrate lyase (EC 4.1.3.6), has been adapted and evaluated for use with clinical samples. Membrane filters removed serum proteins, which interfere with the analysis, and reagent and sample volumes were decreased from those in the manufacturer's protocol, thereby decreasing the cost of the assay. Using gravimetrically prepared citrate standards, we determined that assay results varied linearly with concentration up to sixfold the upper reference limit for serum citrate. Intra- and interassay variation were within acceptable limits (CVs less than 3% and less than 8.5%, respectively). Kit reagents were stable for four weeks at -20 degrees C. Assay results were unaffected by hemolysis or other biochemical interferences. The method evidently provides a rapid, convenient microassay for citrate in clinical samples.

Bilirubin↗

PubMed1984

Polymorphonuclear leukocytic inhibition by citrate, other metal chelators, and trifluoperazine. Evidence to support calcium binding protein involvement.

Corneal ulceration after severe alkali burns of the eye is thought to result principally from collagen breakdown as a consequence of local polymorphonuclear leukocyte (PMN) activities. The favorable effect of topical citrate on such burns suggested a direct effect on these inflammatory cells. These in vitro studies show that the stimulation of human PMN by opsonized zymosan can be inhibited by citrate, EDTA, and EGTA. These compounds interfere with opsonized zymosan attachment to PMN, preventing the respiratory burst, phagocytosis, and degranulation. Reversal of this inhibition by calcium and/or magnesium suggests that mechanism is calcium chelation. Trifluoperazine (TFP) inhibition of opsonized zymosan attachment and phagocytosis implicates the involvement of calmodulin. We propose that citrate, EDTA, and EGTA interfere with the receptor mediated attachment of opsonized zymosan to the PMN cell membrane, leaving the PMN in a resting, granulated state. Inhibition of the receptor system by calcium depletion may be the result of interference with calcium-calmodulin modulated microfilament and/or microtubule interfaces in the PMN plasma membrane. It is postulated that comparable events occur in the citrate treated alkali burned cornea. Citrate inhibition of PMN may be useful in other eye and systemic diseases.

Burns↗

PubMed1981

Sodium citrate reduces the incidence of corneal ulcerations and perforations in extreme alkali-burned eyes--acetylcysteine and ascorbate have no favorable effect.

Alkali-burned eyes (45 sec, 12 mm, 4N NaOH) were subjected to topical treatment with 10% ascorbate, 20% acetylcysteine, 10% ascorbate together with 20% acetylcysteine, 10% citrate, or Adsorbotear vehicle. Only citrate-treated eyes showed a significant decrease in corneal ulcerations and perforations (17%) compared with ascorbate (88%), acetylcysteine (81%), ascorbate/acetyl-cysteine (100%), or Adsorbotear (75%). In the citrate-treated eyes there was a significantly reduced incidence of band keratopathy (17%) but an increased incidence of hyphema (100%). Both groups receiving acetylcysteine developed acellular corneal caps, the result of peripheral ulceration undermining the central cornea. Polymorphonuclear neutrophils (PMN) were substantially increased at the base of the cap in the acetylcysteine- and acetylcysteine/ascorbate-treated eyes at day 56. At the end of the experiment, citrate-treated eyes showed substantially fewer stromal PMN than any other group. These results show that topical citrate has a most favorable effect on the incidence of corneal ulceration and perforation after alkali burning.

Acetylcysteine↗

PubMed1981

[Changes in the pump function of the right ventricle during "pressure-autotransfusion" with citrate and heparin (author's transl)].

Nine anaesthetized, splenectomized dogs, heparinized with 300 IU/kg bodyweight heparin i.v. had one tenth of their total blood volume returned to them by autotransfusion under maximum pressure with the Bentley-system. For the "Heparin"-autotransfusion (n = 49) 1:5 0,9% NaCl was added to the blood; whilst for the "Citrate"-autotransfusion 1:5 ACD-B(n = 28) or CPD (n = 30) stabilisor was added. Autotransfusion was performed as follows: Heparin-ACD-B- Heparin-DPD- Heparin-ACD-B etc. The pump function of the right ventricular myocardium was measured by the force of contraction (PRV, IP, SV, T1) as well as by criteria of contractility (dp/dtmax, VCEmax, KI1, KI2). Immediately after acute bleeding a reduction of the force of contraction to 50% was seen, but the contractility remained unchanged. During the maximum pressure autotransfusion of the blood the force of contraction consistently increased irrespective of the anticoagulant used. The contractility remained unchanged. In the following phase the force of contraction and the contractility normalised when heparin was employed, whilst when citrate was used there was a reduction of the force of contraction and of the contractility corresponding with the different dose of citrate of ACD-B and CPD. This short phase was followed by spontaneous stabilisation of the circulation. The force of contraction and the contractility returned to normal when heparin and ACD-B were employed, whilst a reduction of these criteria occurred when CPD was used. From these findings, the scheme of anticoagulation for citrate under clinical conditions should be modified by a prior injection of 2,000-3,000 IE of heparin i.v. and the addition of citrate in the ratio of 1:7 for ACD-B or 1:8 for CPD.

Animals↗

PubMed1980

Studies on human heart citrate synthase.

Citrate synthase from human heart was purified by affinity chromatography with Sepharose-ATP. The molecular weight (100,000) and the presence of two presumably identical subunits do not differ from other mammalian citrate synthases. However, the kinetics constants and immunologic characteristics of the enzyme differed from other mammalian citrate synthases. The Km values for acetyl-CoA (0.4 microM) and oxaloacetate (0.25 microM) were about an order of magnitude lower than those previously found for other mammalian (and eucaryotic) citrate synthases. The kinetics constants for the reverse reaction Km for citrate (420 microM) and CoA (70 microM), were of similar magnitude to the values for other mammals. Anti-human heart antiserum developed a single precipitin line in an Ouchterlony plate against a heart extract, no precipitin line with brain, and a precipitin line with spurs against liver and kidney extract. Following myocardial infarction in men, the enzyme appeared in peripheral blood rarely and in low concentration in contrast with earlier experiences with experimental infarction in dogs.

Animals↗

PubMedDate not supplied

[Features of pyruvate and lactate metabolism in tumor-bearing rats following citrate administration].

Everyday administration of citrate (250 mg/kg of body mass) into healthy rats within 4 days inhibited activities of pyruvate kinase, pyruvate dehydrogenase, alanine transaminase and of reverse lactate dehydrogenase in liver tissue but not in sceletal muscles. Within the longer period of citrate administration (8 or 12 days) activities of pyruvate dehydrogenase and alanine transaminase continued to decrease in liver tissue, at the same time, content of pyruvate proceeded to increase in sceletal muscles. More distinct inhibitory effect of citrate on the pyruvate dehydrogenase activity was observed not only in liver tissue but and in sceletal muscles of tumor-bearing animals. Alanine transaminase, which was inactivated in liver tissue of healthy animals after citrate treatment, was markedly activated in tumor-bearing rats in the same conditions. The data obtained suggest that some regulatory functions of citrate were qualitatively transformed in tumor-bearing animals, mainly, in relation to turnover of glucogenic amino acids.

Alanine Transaminase↗

PubMed1978

[The effect of citrate or heparin coagulation on the dog's heart work in autotransfusion].

During massive autotransfusion in the dog, the different anticoagulation processes have an important influence on heart work and performance. This is especially marked with citrate, depending on the amount and the transfusion rate. In spite of normovolemia both parameters show a transient decrease up to 40% - 50% with ACD and up to 60% - 70% with CPD. These different reactions may be due to the corresponding composition of each stabilizer. The effect is abolished by simultaneous use of citrate and calcium, which may prove that the observed changes are caused mainly by a depletion of ionized calcium caused by the rapid transfusion. This is comparable to the well-known citrate intoxication. In contrast both cardiac parameters decrease only about 10% with heparin anticoagulation. Heparinization seems to be preferable to citrate as regards heart work and performance during massive autotransfusion. Also the two citrate stabilizers significantly differ in their effect on both cardiac parameters, the use of ACD being favoured.

Animals↗