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At least 1,063 records · Page 59Linked to original sources
PubMed2005

Sildenafil citrate (Viagra) enhances vasodilatation in fetal growth restriction.

BACKGROUND: Fetal growth restriction (FGR) affects up to 8% of all pregnancies and has massive short-term (increased fetal morbidity and mortality) and long-term (increased incidence of cardiovascular disease in adulthood) health implications. Doppler waveform analysis of pregnancies complicated by FGR suggests compromised uteroplacental circulation and placental hypoperfusion. Our aim was to determine whether myometrial small artery function was aberrant in FGR and to assess whether sildenafil citrate could improve vasodilatation in FGR pregnancies. METHODS: Small arteries dissected from myometrial biopsies obtained at cesarean section from normal pregnant women (n = 27) or women whose pregnancies were complicated by FGR (n = 12) were mounted on wire myographs. Vessels were constricted (with arginine vasopressin or U46619) and relaxed (with bradykinin) before and after incubation with a phosphodiesterase-5 inhibitor, sildenafil citrate. RESULTS: We demonstrated increased myometrial small artery vasoconstriction and decreased endothelium-dependent vasodilatation in vessels from women whose pregnancies were complicated by FGR. Sildenafil citrate significantly reduced vasoconstriction and significantly improved relaxation of FGR small arteries. CONCLUSIONS: We conclude that sildenafil citrate improves endothelial function of myometrial vessels from women whose pregnancies are complicated by intrauterine growth restriction. Sildenafil citrate may offer a potential therapeutic strategy to improve uteroplacental blood flow in FGR pregnancies.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Effects of acute and chronic coingestion of AlCl3 with citrate or polyphenolic acids on tissue retention and distribution of aluminum in rats.

Aluminum (Al) is toxic to certain biological systems and has been implicated as a neurotoxic agent in the pathogenesis of Alzheimer's disease. Intestinal absorption of Al is very low (0.1%), but many organic dietary components are potential chelators of Al and may enhance its absorption and tissue distribution. We examined the effects of acute and chronic coingestion of AlCl3 with different polyphenolic acids on Al retention and compared to citrate in rats. In experiment 1, animals fasted for 14 h were dosed orally with demineralized water, Al chloride, Al chloride plus sodium citrate, or Al chloride plus a polyphenol acid. Blood samples were taken before and 2 h after the gavage and animals were killed 6 h later. In experiment 2, the rats were adapted on a purified diet for 1 wk and received the following for 4 wk in their experimental diets: AlCl3, except group 1, plus citrate or a polyphenol acid, except groups 1 and 2. Animals were killed and blood and tissues were sampled. In experiment 1, citrate highly enhanced Al absorption and its tissue retention. Gallic and chlorogenic acids significantly increased tibia and kidney Al levels compared to the Al group. In experiment 2, Al levels in the urine were significantly increased in all the Al groups compared to the control group. Significantly higher Al levels in the tibia, kidney, and brain were observed in the citrate group and a significant increase in brain Al level was also noted in the chlorogenic acid group compared to AlCl3 group. This may suggest a possible relation structure-activity of polyphenol acids. However, further studies are necessary to better understand the influence of polyphenol acids on Al metabolism, in particular that of chlorogenic acid.

Aluminum↗
PubMed1985

Sodium, potassium, calcium, magnesium, zinc, citrate and chloride content of human prostatic and seminal fluid.

The ionic composition of human prostatic fluid varied greatly between individuals, reflecting the secretory activity of the gland and the presence or absence of prostatic inflammatory disease. In normal prostatic fluid the major anion was citrate, while chloride concentrations were lower. Their counterions were mainly sodium and potassium, together with calcium, magnesium and zinc. Prostatic secretions from men with prostatitis comprised mainly sodium and chloride. The electrolytes were closely correlated to each other (except for sodium, which was essentially invariant at about 145 nm). The molar changes per mole of citrate were about 0.52, potassium; -0.53, chloride; 0.17, calcium; 0.14, magnesium; and 0.09, zinc. The pH was also associated with citrate, decreasing from 8.0 to 6.2 as the citrate increased. These various ionic changes can be explained as responses to citrate secretion, without the need to propose specific transport mechanisms for the other ions measured. The marked effect of prostatic inflammation on the composition of prostatic fluid can be seen as being due mainly to decreased secretion rather than active modification.

Calcium↗
PubMed1992

Purification of an embryotrophic factor from commercial bovine serum albumin and its identification as citrate.

A factor of low M(r) with growth-promoting effects on rabbit embryos was extracted and purified from commercial bovine serum albumin (BSA). This embryotrophic factor was extracted from BSA dissolved in formic acid by membrane filtration (membrane cutoff of M(r) 10,000) and then freeze-drying of the filtrate. The extract was purified successively by chromatography on G-10 Sephadex, QAE-Sephadex A-25 anion exchange and high-performance liquid chromatography (HPLC) reverse-phase columns. Mass spectrometry of the active reverse-phase material indicated that the major component in this material had an M(r) of 192. The embryotrophic factor in the low M(r) extract of BSA was shown to be citrate, because: (i) the mass spectra of the active reverse-phase material and citrate were identical, (ii) the activity was eluted at the identical position to citrate on an analytical HPLC anion-exchange column, (iii) the original BSA sample was shown by enzyme assay to be heavily contaminated by citrate and (iv) citrate stimulated cell proliferation and expansion of blastocysts.

Animals↗
PubMed1975

The effects of age and fluoride exposure on fluoride, citrate and carbonate content of human cementum.

A study was conducted to determine the values of several chemical components of dental cementum. Extracted teeth from continuous residents of low, optimal, and high natural fluoride areas were selected to determine the effects of fluoride exposure and age on the fluoride, citrate and carbonate content of cervical and apical areas of sound and periodontally diseased human cementum. 1. For normal cementum the mean fluoride content of all 18 groups was 0.443 plus or minus 0.04%on an ash basis and 0.253 plus or minus 0.02% on a dry weight basis; the mean citrate content was 1.52 plus or minus 0.10% on an ash basis and 0.86 plus or minus 0.06% on a dry weight basis; the mean carbonate content was 4.95 plus or minus 0.39% on an ash basis and 2.79 plus or minus 0.22% on a dry weight basis. 2. For diseased cementum the mean fluoride content of all 12 groups was 0.575 plus or minus 0.03% on an ash basis and 0.342 plus or minus 0.02% on a dry weight basis; the mean citrate content was 1.19 plus or minus 0.07% on an ash basis and 0.71 plus or minus 0.05% on a dry weight basis; the mean carbonate content was 5.95 plus or minus 0.47% on an ash basis and 3.50 plus or minus 0.28% on a dry weight basis. 3. There is a general increment in fluoride content of normal cervical and apical cementum, both with age and fluoride exposure. For diseased cementum this held true for fluoride exposure but not age. 4. The mean fluoride content of cervical cementum is greater than that of apical cementum for both normal and diseased groups. For citrate and carbonate no definite statistical differences were noted between cervical and apical areas. 5. The diseased cementum has a significantly higher mean fluoride content, a significantly lower citrate content, and a slightly, but not statistically significant, higher carbonate content than normal cementum. 6. Unlike bone, no inverse fluoride/citrate or fluoride/carbonate relationship was observed. 7. For both normal and diseased groups the carbonate content of cementum of individuals over age 40 tended to be lower than for individuals 20-40 years of age.

Adolescent↗
PubMed1997

Citrate uptake by isolated rat renal brush border membrane vesicles in cadmium-intoxicated rats.

Epidemiological Studies have reported that the formation of renal stones is often observed in workers exposed to cadmium (Cd). Citrate is known to be a protective factor against renal stone formation. We previously reported that direct exposure to high-level cadmium impaired the citrate uptake by the brush border membrane vesicles (BBMV), which may mean that the formation of renal stones from exposure to Cd could be prevented. In the present study, to clarify the mechanism of Cd-induced renal stone formation, the characteristics of BBMV-induced citrate uptake were determined in Cd-intoxicated rats. Cd intoxication was induced by daily subcutaneous injections of CdCl2 at a dose of 2 mg Cd/kg body wt per day for 17 to 20 days. The BBMV were prepared by the divalent cation precipitation method. Citrate uptake was measured by the Millipore rapid membrane filtration technique. The citrate uptake per mg protein was not significantly different between the two groups. The volume of BBMV was significantly reduced (50%) in Cd-intoxicated rats compared with that of control rats. Percentages of the equilibrium value were also significantly inhibited in Cd-intoxicated rats.

Animals↗
PubMed1981

Myocardial release of citrate and lactate during atrial pacing-induced angina pectoris.

Arterio-coronary sinus (A-Cs) differences of plasma citrate, glucose, free fatty acids and blood lactate were measured in 19 patients with coronary artery disease (CAD) and in eight control subjects exposed to atrial pacing. Among patients with CAD 11 showed a myocardial release of lactate during pacing (lactate producers, LP) while myocardial lactate extraction was unchanged in the remaining eight patients (lactate non-producers, LNP). In patients with CAD, (A-Cs) plasma citrate differences became increasingly negative during recovery from pacing, values at rest and at 3-5 min of recovery were: -5 +/- 2 mumol/l (mean +/- SD) vs. -12 +/- 5 mumol/l in LP (P less than 0.001) and -6 +/- 3 mumol/l vs. -8 +/- 4 mumol/l in LNP (P less than 0.01). In controls, (A-Cs) citrate difference varied inversely, from -8 +/- 4 mumol/l at rest to -2 +/- 4 mumol/l at 3-5 min of recovery (P less than 0.001). An increasingly negative (A-Cs) plasma citrate difference during recovery from pacing-induced angina pectoris is suggested to reflect a wash-out of accumulated citrate from ischaemic heart cells; and is proposed as a more sensitive marker of ischaemia in man than a myocardial release of lactate.

Adult↗
PubMed1994

Induction of hepatic ATP-citrate lyase by insulin in diabetic rat--effects of insulin on the contents of enzyme and its mRNA in cytosol, and the transcriptional activity in nuclei.

The effects of insulin on ATP-citrate lyase, its mRNA in cytosol, and the transcriptional activity in nuclei of diabetic rat liver were studied. Experimental diabetes was induced by an intraperitoneal injection of streptozotocin, and livers were removed from rats at 0, 1, 3, 6, 16, and 72 hours after the administration of insulin. ATP-citrate lyase began to increase at 16 hours, and continuously increased until 72 hours. The amount of mRNA encoding ATP-citrate lyase increased abruptly at 16 hours, then decreased to near basal level in 72 hours. No change in the transcription rate was observed until 3 hours after insulin administration. However, the activity increased 4-fold at 6 hours and 7-fold at 16 hours, 16-fold at 6 hours and 28-fold at 16 hours when pGACL1 and pGACL2 were used as probes, respectively, preceding the increase in the amounts of mRNA and the enzyme. It is suggested that the increase in the amount of ATP-citrate lyase by insulin is primarily due to the increase in the transcriptional activity of the gene in nuclei, which results in the subsequent increase in the amount of mRNA for the biosynthesis of ATP-citrate lyase in cytosol.

ATP Citrate (pro-S)-Lyase↗
PubMed1999

Segmental colonic transit after oral 67Ga-citrate in healthy subjects and those with chronic idiopathic constipation.

UNLABELLED: Measurement of segmental colonic transit is important in the assessment of patients with severe constipation. 111In-diethylenetriamine pentaacetic acid (DTPA) has been established as the tracer of choice for these studies, but it is expensive and not readily available. 67Ga-citrate is an inexpensive tracer and when given orally is not absorbed from the bowel. It was compared with 111In-DTPA in colonic transit studies in nonconstipated control subjects and then in patients with idiopathic constipation. METHODS: Studies were performed after oral administration of 3 MBq (81 microCi) 67Ga-citrate or 4 MBq (108 microCi) 111In-DTPA in solution. Serial abdominal images were performed up to 96 h postinjection, and computer data were generated from geometric mean images of segmental retention of tracer, mean activity profiles and a colonic tracer half-clearance time. RESULTS: There were no differences in segmental retention of either tracer or in mean activity profiles between control subjects and constipated patients. Results in constipated subjects were significantly different from those in controls. The mean half-clearance times of tracer for control subjects were 28.8 h for 67Ga-citrate and 29.9 h for 111In-DTPA in control subjects and 75.0 h for 67Ga-citrate and 70.8 h for 111In-DTPA in constipated patients. CONCLUSION: Oral 67Ga-citrate can be used as a safe alternative to 111In-DTPA for accurate measurement of segmental colonic transit.

Administration, Oral↗
PubMed1999

Effects of citrated whole blood transfusion in response to hemorrhage.

BACKGROUND AND PURPOSE: Standard treatment for massive hemorrhage in dogs is infusion of whole blood or of packed red blood cells with fresh frozen plasma if whole blood is not available. Although most whole blood is collected using a citrate-based anticoagulant, knowledge of citrate's relevant non-anticoagulant effects is not widespread. Citrate's anticoagulant activity is achieved through chelation of divalent metal cations (e.g., magnesium, calcium), which may exacerbate cardiovascular and metabolic insults attributable to hemorrhage. METHODS: Blood pressures, gas tensions, metabolites, and electrolytes; myocardial metabolites, pressures, and contractility; cardiac output; and left cranial descending and circumflex coronary artery flows were measured in 21 anesthetized dogs after hemorrhage was induced by collection of blood into a citrated reservoir to mean arterial pressure of 45 mm Hg for approximately 60 min (until arterial lactate concentration was 7.0 mmol/L), followed by a 1-h transfusion and 2 h of maintenance. RESULTS: Arterial ionized calcium concentration, total peripheral resistance, and myocardial function decreased significantly during hemorrhage. All aforementioned responses but myocardial function continued to decrease during the initial 20 min of transfusion, then began to recover. Total peripheral resistance and end-systolic elastance were the only factors significantly related to calcium concentration. CONCLUSION: Transfusion with citrated whole blood may significantly alter calcium concentration, negatively affecting myocardial and vascular function.

Animals↗
PubMed1975

The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia.

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.

Animals↗
PubMed2001

[Therapeutic use of potassium citrate].

Therapeutic indications of potassium citrate include: 1. Oxaluric renal stone disease and some cases of uric acid stone disease. Prevention of stone formation in patients with renal polycystic disease. Prevention of stone relapse after ESWL or lithotomy; 2. Distal renal tubular acidosis complicated by hypercalciuria, mainly in children. 3. Renal hypercalciuria and hyperoxaluria. 4. Prevention of renal complications at the time of glaucoma treatment with acetazolamide. 5. Potassium supplementation during treatment of hypertension. Potassium citrate is usually contraindicated in the case of: 1. Urinary tract infection. 2. Struvite renal stone disease. 3. Hyperpotassemia and advanced chronic renal failure. 4. Peptic ulcer or gastritis. 5. Gastrointestinal bleeding. 6. Disorders of coagulation, crural varices. 7. Metabolic alkalosis. Potassium citrate, when used at therapeutic doses, is to be considered as quite safe. The average daily dose even if admitted as a single dose day engages 60-75% of free renal capacity for potassium excretion. Physiologic and therapeutic citrate concentration in urine exceeds much those available for other inhibitors. The therapeutic dose does not induce any significant changes in any biochemical or endocrine parameter of blood except mild transient metabolic alkalosis. The decrease of urine calcium and increase in oxalate calcium phosphate excretion is observed. In hypo-cytriaturic patients the response to therapeutic dose of citrate is smaller. One-year remission of stone disease is observed in 70-75% cases.

Acetazolamide↗
PubMed1992

Cloning and nucleotide sequence of the gene (citC) encoding a citrate carrier from several Salmonella serovars.

The nucleotide sequence of the citC coding for the citrate carrier in several Salmonella serovars has been determined, and the amino acid sequence of the carrier protein was deduced. The predicted citrate carrier from Salmonella pullorum and Salmonella enteritidis consists of 446 amino acids with a molecular weight of 47,621, whereas that from Salmonella dublin is the same 446 amino acids with the slightly different molecular weight of 47,591, because 1 amino acid residue was substituted. The predicted proteins are highly hydrophobic (69% nonpolar amino acids). The hydropathy profile suggests that the proteins are composed of 11-12 hydrophobic membrane-spanning segments with two hydrophilic cores in the middle of the protein sequence. No homology in the nucleotide and amino acid sequences was found in the molecular structures of citA, citP, and tctI genes. The citC-coding citrate transport activity is Na(+)-dependent and specific for citrate only. The transcript from the citC gene was not detected in the total RNA from several Salmonella serovars except S. dublin in Northern blot analysis, although the promoter of the citC genes appeared to be functional in Escherichia coli and Salmonella typhimurium strains using the lacZ fusion assay. These results suggested that the citC gene-coding citrate carrier is probably a TctIII system such as that identified previously in S. typhimurium.

Amino Acid Sequence↗
PubMed2003

Histopathologic effect of chronic use of sildenafil citrate on the choroid & retina in male rats.

BACKGROUND & OBJECTIVES: Sildenafil citrate is an oral medication used to treat male impotence by the inhibition of phosphodiesterase-5 in the corpus cavernosum and subsequent facilitation of penile erection. Though the ocular side effects of sildenafil have been reported, no information is available on the histopathologic effects of chronic use of sildenafil citrate on the ocular vasculature. The present study was undertaken to study the histopathologic effects of chronic use of sildenafil on the retina and choroid of male rats. METHODS: Twelve adult male Wistar rats were used in the study. Six of them were given 8 mg/kg/day sildenafil citrate orally on alternate days, the other six rats were used as control. The animals were sacrificed after 4 wk of treatment, and the eyes were fixed in 10 per cent formalin solution and sectioned after embedding in paraffin. Sections were cut, stained with haematoxylin-eosin (HE) or periodic acid Schiff (PAS) and examined under light microscope. The choroidal capillary diameter was also measured. RESULTS: The choroidal capillaries were more dilated in the sildenafil citrate treated group (mean capillary diameter 3.44 +/- 1.68 microm versus the control of 1.78 +/- 1.36 microm, P < 0.001). The retinal layers and their configuration were unchanged in both the groups. INTERPRETATION & CONCLUSION: Chronic use of sildenafil citrate can cause dilatation and congestion in the choroidal vasculature of male rats.

Animals↗
PubMed2006

[Urinary citrate excretion in children with calcium urolithiasis].

UNLABELLED: Citrate is thought to be one of the most important inhibitor of calcium salts crystallization in the urine. Therefore, an assessment of urinary citrate excretion is an integral element of metabolic evaluation in urolithiasis. The reported incidence of urolithiasis associated with hypocitraturia varies from 10% to 63%. The purpose of the study was to assess urinary citrate excretion in children with calcium urolithiasis living in region of Lublin. The study comprised 60 children (34 boys and 26 girls) aged 4.3-18 years. In 36 of them, calcium oxalate urolithiasis was diagnosed by spectrophotometry. In the remaining children, an assessment of stone composition was impossible. However, in all children, stones were radiopaque. Hypercalciuria (HC) and mild hyperoxaluria (HOx) were diagnosed in 23 and 16 children, respectively. In the remaining 21 children urolihiasis was classified as idiopathic. The controls were 35 healthy age- and gender-matched children. Urinary citrate excretions were assessed by enzymatic method in 24-hour urine specimens and expressed as citrate/creatinine ratios (Cit/Cr). Decreased Cit/Cr were observed in 9 (15%) children with calcium urolithiasis. However, there was no significant difference between the mean Cit/ Cr in children with calcium urolithiasis and controls (410 +/- 207 mg/g vs 385 +/- 144 mg/g). There was also no significant difference between the mean Cit/ Cr in children with HC and controls. Similarly, the mean Cit/Cr did not differ significantly between children with HOx and controls. However, the lowest mean Cit/Cr was revealed in children with HOx (306 +/- 161 mg/g). CONCLUSIONS: In most children with calcium urolithiasis urinary citrate excretion was normal. However, in some children with urolithiasis, detection of hypocitraturia allows to explain pathogenesis of stone formation and to carry on a causative prophylaxis.

Adolescent↗
PubMed1976

Metabolic effects of some antibilharzial drugs inhibition of citrate oxidation by Bilharcid.

Bilharcid inhibited citrate oxidation and the inhibition was decreased by time. The inhibition is not restored or reduced by increasing citrate concentration. NAD stimulated citrate oxidation in the presence of Bilharcid. Cysteine slightly stimulated citrate oxidation, while ATP had no effect. Addition of citrate before Bilharcid protected the enzyme against the inhibitory action of the drug.

Adenosine Triphosphate↗
PubMed1990

Investigating aluminium citrate speciation by high performance liquid chromatography.

The toxicity of aluminium (Al) is dependent on its chemical form or species. However, there are no current techniques available to separate small molecular weight toxic Al complexes. In the present study, HPLC separation was combined with atomic absorption spectroscopic detection of Al in an attempt to determine the potential for this analytical method to separate Al citrate from other Al species. A total of nine different HPLC stationary phase supports along with numerous mobile phases were examined. Promising results were obtained with the Cyclobond I and Cyclobond III columns containing the beta- and alpha-cyclodextrin stationary phases, respectively and the cyano column. Using a mobile phase of methanol:water (1:1; v/v) containing 0.1 M triethylamine (TEA) and glacial acetic acid (pH = 4.0), Al was reproducibly retained for approximately 9 minutes following the injection of Al citrate onto the Cyclobond III column. Injection of other simple Al complexes showed no demonstrable recovery of Al under these same conditions. However, the more stable Al desferrioxamine complex was retained, but with a retention time that was only 3-4.5 minutes. Unfortunately, the retention characteristics and recovery of Al were not reproducible or sufficient with either of the cyclobond columns for routine quantitation of Al citrate in biological samples. The cyano column did provide better recovery of Al citrate (up to 65%) than could be obtained with the cyclobond column (up to 58%). However, manipulation of the retention time for Al citrate on the cyano column was limited to a period of only 3-4.5 minutes. Under similar conditions, Al desferrioxamine could be retained for over 10 minutes on this same column.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMedDate not supplied

Cardiac arrest after hypertonic citrate anticoagulation for chronic hemodialysis.

The use of regional citrate anticoagulation as an alternative to standard therapy in hemodialysis patients at risk for bleeding complications has been well described. Recently, a method using hypertonic citrate has been reported as being safe and efficacious, and having several advantages over the usual techniques. Two patients who suffered cardiac arrests after dialysis using hypertonic citrate are discussed. Both received anticoagulation as described in the literature, although the citrate infusion rate was lower than recommended. Electrocardiograms obtained during the first such session showed no change in the Q-Tc interval with initiation of the infusion in either patient. Both were noted to have cardiac arrest within 5 minutes of discontinuation of dialysis, without warning symptoms, following the second and fifteenth treatments, respectively. The initial rhythm of ventricular fibrillation did not respond to standard advanced cardiac life support therapy, and the patients were not successfully resuscitated until they received intravenous calcium. The authors postulate that the loss of positive calcium flux from the dialysate, in conjunction with circulating unmetabolized citrate, caused an electrolyte imbalance leading to the potentially fatal arrhythmia. Caution is recommended in using this method of regional anticoagulation.

Adult↗