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At least 649 records · Page 36Linked to original sources
PubMed1985

Sodium citrate pretreatment in elective cesarean section patients.

Thirty-two healthy term parturients undergoing elective cesarean section randomly received either no antacid (n = 10), 30 ml of 0.3 molar sodium citrate less than 60 min preoperatively (n = 11), or 30 ml of 0.3 molar sodium citrate longer than 60 min preoperatively (n = 11). Immediately after delivery, the stomach was emptied as completely as possible through a #18 Salem Sump tube passed orally. Mean gastric pH in the three groups was 1.8 +/- 2.7 (SD), 5.0 +/- 1.5, and 2.7 +/- 1.2, respectively. Gastric pH was significantly higher in the short interval group than in either the control group or in patients receiving their sodium citrate more than 60 min in advance. Gastric volumes were similar. All control patients had a gastric pH less than 2.5. Nine percent of patients receiving sodium citrate less than 60 min in advance and 50% of patients receiving their sodium citrate longer than 60 min in advance had a pH of less than 2.5. Volumes exceeding 25 ml occurred with equal frequency. No patient in the short interval group had a combination of both pH of less than 2.5 and a volume exceeding 25 ml. This combination occurred with equal frequency in control patients (64%) and in those patients receiving their sodium citrate more than 60 min in advance (50%). We conclude that sodium citrate effectively increases gastric pH when given less than 60 min prior to the induction of anesthesia.

Adult↗
PubMed1982

AMP deaminase as a control system of glycolysis in yeast. Mechanism of the inhibition of glycolysis by fatty acid and citrate.

The role of fatty acid and citrate on the interaction of the AMP deaminase (EC 3.5.4.6) reaction with glycolysis was investigated using permeabilized yeast cells. (a) Linolenate and citrate inhibited glycolytic flux and the recovery of the adenylate energy charge; however, linolenate remarkably retarded the depletion of the total adenylate pool, which was not at all affected by the addition of citrate. (b) Linolenate inhibited AMP deaminase activity in situ, resulting in the subsequent decrease in ammonium production, which reduced the activity of 6-phosphofructokinase (EC 2.7.1.11), whereas linolenate itself had no ability to inhibit the phosphofructokinase activity in the presence of excess ammonium concentration. (c) Citrate inhibited the activity of phosphofructokinase in situ in the presence and absence of ammonium ion, followed by an inhibition of glycolysis; however, AMP deaminase activity was not inhibited by citrate. The inhibition of glycolysis by fatty acids can be accounted for by the lowered activity of phosphofructokinase as a result of the decreased level of ammonium ion through the inhibition of the AMP deaminase reaction by these ligands, whereas the effect of citrate on glycolysis is a direct inhibition of phosphofructokinase without affecting the activity of AMP deaminase. Fatty acid and citrate, a principal metabolic product of fatty acid oxidation, can be responsible for the control of glycolysis in two different manners.

AMP Deaminase↗
PubMed1978

Isocitrate uptake and citrate production by rat ventral prostate fragments.

Prostatic aconitase was investigated utilizing fragments of rat ventral prostate. The rate of citrate formation from isocitrate was used as an index of aconitase activity. Inhibition of citrate formation from isocitrate by fluorocitrate indicated that aconitase activity was being measured. The results indicated that whereas both kidney and prostate formed citrate from isocitrate, the aconitase activity of prostate was independent of both medium isocitrate and citrate concentration. In addition the aconitase activity of prostate seemed to favor citrate formation to a much greater degree than kidney. The results showed that the aconitase catalyzed conversion of citrate to isocitrate is limited in prostate and suggested that the deficient citrate oxidation observed in prostate is the result of a unique aconitase activity.

Aconitate Hydratase↗
PubMed1982

Enzymic determination of citrate in serum and urine, with use of the Worthington "ultrafree" device.

We describe an enzymic method for conveniently measuring citrate in serum or urine. Interfering enzyme proteins are removed by a disposable ultrafilter ("Ultrafree"; Worthington Diagnostics), obviating the need for hazardous protein precipitants. A 50 mmol/L Tris buffer adequately controls pH, no lactate dehydrogenase is necessary in the reagents, and the reaction of citrate catalyzed by citrate lyase (EC 4.1.3.6) is complete in 2-3 min. Within-run and day-to-day coefficients of variation were 7.5% and 5.4%, respectively. Serum citrate concentrations for 20 apparently healthy persons ranged from 0.08 to 0.17 mmol/L (mean 0.12, SD 0.03). Urinary citrate excretion by six normal volunteers ranged from 2.2 to 4.4 mmol/24 h. We observed no detectable changes in citrate in whole blood stored at room temperature for 90 min or longer. Overall, the method is faster and less hazardous than other methods for citrate that require protein precipitation.

Citrates↗
PubMed1995

Mitochondrial citrate synthase from potato: predominant expression in mature leaves and young flower buds.

A cDNA clone encoding mitochondrial citrate synthase (EC 4.1.3.7), the first enzyme of the tricarboxylic-acid cycle, was isolated from potato (Solanum tuberosum L.) and expression of the enzyme analyzed. The deduced amino-acid sequence of the potato mitochondrial citrate synthase showed high similarity to known citrate synthases from fungi, mammals and Arabidopsis thaliana. The expression pattern of this clone was determined by Northern blot analysis. Expression was detected in all tissues analyzed. The highest level of expression was found in green flower buds. In photosynthetic tissues, stronger mRNA expression was detected in mature than in immature leaves. This rise in expression with leaf age was accompanied by an increase in citrate-synthase activity. Within flowers, expression was severalfold stronger in anthers than in ovaries, indicating a role of mitochondrial citrate synthase during anther or pollen development. A comparatively low level of transcript was detected in underground heterotrophic tissues, such as stolons, tubers and roots. When tubers were stored at low temperature (4 degrees C), mitochondrial citrate-synthase gene expression increased slightly. From the data obtained, we conclude that expression of the mitochondrial citrate-synthase gene is regulated by developmental and environmental factors. The relatively high expression in leaves is in line with the assumption that mitochondria play an important role in photosynthetically active tissues.

Amino Acid Sequence↗
PubMed1993

Studies on the reduction of aortic calcification by alkali citrates in an ex vivo tissue preparation in the rat.

The effect of orally administered alkali citrates on the calcification of arterial vessel was studied in the rat. Freshly dissected aortic segments were placed in Millipore diffusion chambers and grafted intraperitoneally. Within 21 days calcification of the media had developed. Under treatment with 2.1 mmol citrate per animal and day a significant decrease in histologically detectable calcification areas occurred, as assessed by greatest thickness and longitudinal expansion. This effect was more pronounced with potassium citrate and potassium sodium citrate, and less marked with sodium citrate. The calcium and phosphorus content of aortic tissue remained unchanged, but magnesium increased significantly. The spheroid particles deposited in the media were characterized in more detail by electron microscopy and elemental microanalysis, X-ray diffraction, and determination of the molar calcium-phosphorus ratio. The combined data suggest that in the model selected for studying biocalcification not mature hydroxyapatite but some precursor of this substance is deposited, and that in animals receiving alkali citrate treatment deposition of amorphous calcium phosphate is likely. It is concluded that in the ex vivo aortic wall preparation oral alkali citrates a) bring about a reduction in calcification areas in the media layer, b) impair the maturation of hydroxyapatite and its deposition in the arterial tissue; c) promote the accumulation of magnesium. Whether these results are of significance for the calcification of arteries in situ and treatment regimens is unknown.

Animals↗
PubMedDate not supplied

Anaerobic citrate metabolism and its regulation in enterobacteria.

Several species of enterobacteria are able to utilize citrate as carbon and energy source. Under oxic conditions in the presence of a functional tricarboxylic acid cycle, growth on this compound solely depends on an appropriate transport system. During anaerobiosis, when 2-oxoglutarate dehydrogenase is repressed, some species such as Klebsiella pneumoniae and Salmonella typhimurium, but not Escherichia coli, are capable of growth on citrate by a Na+-dependent pathway forming acetate, formate, and CO2 as products. During the last decade, several novel features associated with this type of fermentation have been discovered in K. pneumoniae. The biotin protein oxaloacetate decarboxylase, one of the key enzymes of the pathway besides citrate lyase, is a Na+ pump. Recently it has been shown that the proton required for the decarboxylation of carboxybiotin is taken up from the side to which Na+ ions are pumped, and a membrane-embedded aspartate residue that is probably involved both in Na+ and in H+ transport was identified. The Na+ gradient established by oxaloacetate decarboxylase drives citrate uptake via CitS, a homodimeric carrier protein with a simultaneous-type reaction mechanism, and NADH formation by reversed electron transfer involving formate dehydrogenase, quinone, and a Na+-dependent NADH:quinone oxidoreductase. All enzymes specifically required for citrate fermentation are induced under anoxic conditions in the presence of citrate and Na+ ions. The corresponding genes form a cluster on the chromosome and are organized as two divergently transcribed operons. Their co-ordinate expression is dependent on a two-component system consisting of the sensor kinase CitA and the response regulator CitB. The citAB genes are part of the cluster and are positively autoregulated. In addition to CitA/CitB, the cAMP receptor protein (Crp) is involved in the regulation of the citrate fermentation enzymes, subjecting them to catabolite repression.

Anaerobiosis↗
PubMed1976

Accumulation of neutral lipids in Saccharomyces carlsbergensis by myo-inositol deficiency and its mechanism. Reciprocal regulation of yeast acetyl-CoA carboxylase by fructose bisphosphate and citrate.

The abnormal accumulation of lipids due to myo-inositol deficiency in Saccharomyces carlsbergensis, and the mechanism involved was investigated. The deficient cells contained much more neutral lipids with a greater ratio of unsaturated fatty acids compared to the supplemented cells, whereas there was no significant change in their phospholipid contents. The biosynthesis of fatty acids and sterols from acetate, and of triacylglycerols and sterol esters from palmitate was markedly augmented in the deficient cells. Acetyl-CoA carboxylase activity of the deficient supernatant was 2- to 5-fold higher than that of the supplemented. However, the activity from both sources was not significantly different after Sephadex G-25 gel filtration of the supernatant, suggesting the presence of low molecular effector(s) in the deficient supernatant. There was a great increase in acid-soluble glycogen, trehalose, and fructose-1,6-P2, as well as a drastic decrease in citrate in the deficient cells. Their intracellular levels were calculated so that their effects on acetyl-CoA carboxylase was examined over the range of physiological concentration. Citrate strongly inhibited the enzyme activity of the supernatant, but it had no effect on the preparation after gel filtration. On the other hand, fructose-1,6-P2 stimulated the enzyme activity both before and after gel filtration. The acetyl-CoA carboxylase activity in the gel filtrate was measured as a function of citrate concentration at several fixed concentrations of fructose-1,6-P2. Citrate counteracted the activation by fructose-1,6-P2 in a dose-dependent manner. Citrate lacked the inhibitory effect in the absence of fructose-1,6-P2. It was concluded from these results that neutral lipid accumulation in the deficient cells reflected an increase in the synthesis of fatty acids, at least partly based on an enhancement of acetyl-CoA carboxylase activity, and that the operation of a reciprocal regulation of the enzyme by fructose-1,6-P2 and citrate caused a marked elevation of the enzyme activity in the deficient cells with a high fructose-1,6-P2 level and a low citrate level.

Acetyl-CoA Carboxylase↗
PubMed1998

A citrate-binding site in calmodulin.

Calmodulin (CaM) is a major Ca2+ messenger which, upon Ca2+ activation, binds and activates a number of target enzymes involved in crucial cellular processes. The dependence on Ca2+ ion concentration suggests that CaM activation may be modulated by low-affinity Ca2+ chelators. The effect on CaM structure and function of citrate ion, a Ca2+ chelator commonly found in the cytosol and the mitochondria, was therefore investigated. A series of structural and biochemical methods, including tryptic mapping, immunological recognition by specific monoclonal antibodies, CIDNP-NMR, binding to specific ligands and association with radiolabeled citrate, showed that citrate induces conformational modifications in CaM which affect the shape and activity of the protein. These changes were shown to be associated with the C-terminal lobe of the molecule and involve actual binding of citrate to CaM. Analyzing X-ray structures of several citrate-binding proteins by computerized molecular graphics enabled us to identify a putative citrate-binding site (CBS) on the CaM molecule around residues Arg106-His107. Owing to the tight proximity of this site to the third Ca(2+)-binding loop of CaM, binding of citrate is presumably translated into changes in Ca2+ binding to site III (and indirectly to site IV). These changes apparently affect the structural and biochemical properties of the conformation-sensitive protein.

Animals↗
PubMed1996

The safety of ranitidine bismuth citrate in controlled clinical studies.

Ranitidine bismuth citrate (Pylorid, Tritec) is a novel drug which heals peptic ulcers and when co-prescribed with either clarithromycin or amoxycillin eradicatesHelicobacter pylori. In controlled clinical studies it was well-tolerated when given alone or when co-prescribed with either antibiotic. Data from 20 clinical studies are reported in this analysis of safety with almost 5000 patients having received ranitidine bismuth citrate (200, 400, or 800 mg twice daily). The incidence of adverse events reported with this new drug, either alone or with an antibiotic, was not different from or lower than in patients given placebo and was independent of the dose of ranitidine bismuth citrate tested. Most commonly reported events (>1% of patients) were upper respiratory tract infection, constipation, diarrhoea, nausea and vomiting, dizziness, and headache, the latter being the only event reported by >2% of patients who received ranitidine bismuth citrate alone. Adverse events considered by the clinical investigator to be adverse reactions occurred with a similar frequency amongst patients given ranitidine bismuth citrate (8%), ranitidine hydrochloride (6%), or placebo (6%). The incidence of adverse reactions was greater when co-prescribed with amoxycillin (11%) or clarithromycin (20%) although it was not different from that noted with the antibiotics alone. Serious adverse events were reported in similar proportions of patients given placebo, ranitidine bismuth citrate alone or with an antibiotic, and ranitidine hydrochloride (range: <1-2%). The safety profile of ranitidine bismuth citrate was thus comparable to that of ranitidine hydrochloride (Zantac), a drug with a well-established record of safety in clinical use.

Journal Article↗
PubMed2005

Endogenous and exogenous citrate transport and release in prostatic preparations: semi-polarized two-dimensional cultures of human PNT2-C2 cells and isolated tubules and segments of rat prostate.

BACKGROUND: Electrophysiological characterization of normal human prostate epithelial cells showed exogenous trivalent citrate transport (release) to be K(+)-dependent. METHODS: (1) Ussing chamber recordings of short circuit current (SCC) were used to study citrate transport in the same (PNT2-C2) cell line grown on micro-pore filters as a monolayer. (2) Release of endogenous citrate from confluent cultures and tubules and segments of rat prostate was measured using a fluorescence technique. (3) Enzyme-spectrophotometry was employed to detect citrate release from segments of rat prostate. RESULTS: Citrate transport across the PNT2-C2 monolayer was asymmetrical, consistent with release into the lumen-side. Fluorescence and/or enzyme-spectrophotometric measurements showed that time-dependent citrate release (endogeneous and preabsorbed) occurred from rat prostate (tubules and segments), but not kidney or lung. The release was dependent on extracellular K(+) but not Na(+). CONCLUSIONS: Citrate release from prostatic cells and tissues (rat and human) was K(+)-dependent, consistent with the previous electrophysiological data.

Animals↗
PubMed1993

Preovulatory administration of clomiphene citrate to mice causes fetal growth retardation and neural tube defects (exencephaly) by an indirect maternal effect.

Clomiphene citrate was administered to female mice at different doses and different times prior to ovulation, in the preimplantation period after ovulation, and after implantation. Pregnancy outcome was determined on day 15 of gestation, when the number of implantations and resorptions were calculated relative to the number of ovulations, and fetuses were assessed for size and stage of development and morphological abnormalities. Preovulatory administration of clomiphene citrate caused decreased implantation rates and growth retardation of surviving fetuses, the degree of the effect being dependent on the dose and the time of drug injection relative to ovulation. The implantation rate was lowest, and the degree of fetal growth retardation highest, when clomiphene citrate was administered immediately before ovulation. An increased incidence of exencephaly was found in the fetuses of females injected with clomiphene citrate prior to ovulation. Transfer of blastocysts from treated mice to untreated fosters showed the effect of clomiphene citrate on implantation and fetal growth to be predominantly mediated through the female reproductive tract, rather than a direct effect on the embryo itself. Administration of clomiphene citrate in the preimplantational period resulted in complete inhibition of implantation, while the only effect when administration was after implantation was a slight reduction in fetal weight. These results indicate that preovulatory clomiphene citrate impairs uterine function, which has an indirect effect on the growth and development of the postimplantation embryo.

Animals↗
PubMed2003

Citrate vs. heparin for anticoagulation in continuous venovenous hemofiltration: a prospective randomized study.

OBJECTIVE: To compare the efficacy and safety of adjusted-dose unfractionated heparin with that of regional citrate anticoagulation in intensive care patients treated by continuous venovenous hemofiltration (CVVH). DESIGN AND SETTING: Prospective, randomized, clinical trial in a 32-bed medical and surgical ICU in a university teaching hospital. PATIENTS: ICU patients with acute renal failure requiring continuous renal replacement therapy, without cirrhosis, severe coagulopathy, or known sensitivity to heparin. INTERVENTIONS: Before the first CVVH run patients were randomized to receive anticoagulation with heparin or trisodium citrate. Patients eligible for another CVVH run received the other study medication in a cross-over fashion until the fourth circuit. MEASUREMENTS AND RESULTS: Forty-nine circuits (hemofilters) were analyzed: 23 with heparin and 26 with citrate. The median lifetime of hemofilters was 70 h (interquartile range 44-140) with citrate anticoagulation and 40 h (17-48) with heparin (p=0.0007). One major bleeding occurred during heparin anticoagulation and one metabolic alkalosis (pH=7.60) was noted with citrate after a protocol violation. Transfusion rates (units of red cells per day of CVVH) were, respectively, 0.2 (0.0-0.4) with citrate and 1.0 (0.0-2.0) with heparin (p=0.0008). CONCLUSIONS: Regional citrate anticoagulation seems superior to heparin for the filter lifetime and transfusion requirements in ICU patients treated by continuous renal replacement therapy.

Acute Kidney Injury↗
PubMed2005

Preventive treatment of nephrolithiasis with alkali citrate--a critical review.

Using the keywords "urolithiasis and citrate treatment", "nephrolithaisis and citrate treatment", "kidney stones and citrate treatment", a Medline search revealed 635 articles published between 1 January 1966 and 1 December 2004. For the present analysis, only studies meeting all of the following criteria were included: (1) publications in English or German, (2) studies on preventive alkali citrate treatment in patients with calcium oxalate, uric acid and infection stone disease, (3) clinical studies including at least ten subjects, and (4) treatment phases of at least 1 week duration. A total of 43 studies met the inclusion criteria and were further subclassified according to intermediate or ultimate endpoints as well as to study design. With stone recurrence as the ultimate endpoint, 21 uncontrolled studies in almost 1,000 patients demonstrated a reduction in stone forming rate by 47-100%. In four randomized controlled trials including 227 patients, 53.5% on alkali citrate vs 35% on placebo remained stone-free after at least 1 year of treatment (P<0.0005). Similar values (66% vs 27.5% for alkali citrate vs placebo, P<0.0005) were obtained in 104 patients from two randomized trials with dissolution/clearance of residual stones as endpoint. Unfortunately, up to 48% of alkali citrate treated patients left the studies prematurely, primarily due to adverse effects such as eructation, bloating, gaseousness or frank diarrhea.

Alkalies↗
PubMed1998

Effect of citrate and pyrophosphate on the stability of calcium oxalate dihydrate.

The effect of citrate and pyrophosphate on the stability of calcium oxalate dihydrate (COD) was studied in an aqueous solution over 7 days. COD was precipitated from 1.0 x 10(-2) mol/l calcium oxalate solution with the addition of citrate and/or pyrophosphate and separated by centrifugation immediately, 48 h and 7 days after the precipitation. The percentage of COD in the precipitate, determined by X-ray diffraction, increased with a rise in citrate or pyrophosphate concentration and reached > or =90% at a citrate concentration of 1.0 x 10(-3) mol/l or a pyrophosphate concentration of 2.0 x 10(-4) mol/l. The resulting COD was completely transformed into calcium oxalate monohydrate within 48 h when the precipitate was composed of <90% COD. Nearly pure COD produced with pyrophosphate was stable over 7 days while that with citrate underwent partial transformation within 48 h. An additive effect of citrate and pyrophosphate was found on the stability of COD. It was concluded that a pyrophosphate concentration above a critical point was sufficient to prevent solution-mediated transformation of COD, and this critical point might be lowered to the physiological range with the presence of citrate.

Calcium Oxalate↗
PubMed1998

The effects of citrate and urinary macromolecules on the aggregation of hydroxyapatite crystals in solutions with a composition similar to that in the distal tubule.

The effects of citrate and dialysed urine (dU) on the aggregation of hydroxyapatite (HAP) crystals in solutions with different pH and otherwise with an ion composition assumed to correspond to that in the distal part of the distal tubule were studied by spectrophotometric assessment of the rate of crystal sedimentation. When the concentration of dU was increased from 1% to 20% we recorded an increased inhibition of HAP crystal aggregation at pH 6.5. There were no differences in the inhibition accomplished by 10% dU when the pH was varied between 5.5 and 7.0, but a lower inhibition was recorded at pH 7.5. Citrate in the range 0.05-4 mmol/l had a concentration-dependent inhibitory effect on HAP crystal aggregation. In the presence of 10% dU the net inhibitory effect of citrate was reduced at all pH levels. In the pH interval 5.5-7.0 a higher inhibition was recorded with 0.5 mmol/l citrate than with 10% dU, but in the presence of dU there was only a minor additional effect of citrate at concentrations below 0.5 mmol/l. These findings indicate that urinary macromolecules present in dU strongly inhibit HAP crystal aggregation under solution conditions corresponding to those in distal tubular urine. At the same nephron level citrate might have a direct inhibitory influence on the aggregation of HAP crystals, but in the presence of normal urinary macromolecules the additive inhibitory effect of citrate is probably only marginal.

Citric Acid↗
PubMed2001

Renal cortical calcification in syngeneic intact rats and those receiving an infrarenal thoracic aortic graft: possible etiological roles of endothelin, nitrate and minerals, and different preventive effects of long-term oral treatment with magnesium, citrate and alkali-containing preparations.

Renal cortical nephrocalcinosis (C-NC) is a rare disorder of uncertain etiology. Using highly inbred (syngeneic) male Lewis rats, we describe the spontaneous occurrence of histologically detectable C-NC in sham operated control rats (Sham; n=12), its aggravation following grafting of the ascending thoracic aorta from a donor rat to the infrarenal aorta of a recipient (ATx; n=12), and differences in C-NC inhibition after 12 weeks of oral administration of magnesium (Mg), citrate and alkali. C-NC is characterized by Kossa-positive areas located in cells of the proximal tubule close to blood vessels and also, to a lesser extent, within glomeruli. After ATx there was vascular overproduction of endothelin (ET-1) but decreased production of nitrate; in renal cortical tissue there was an excess of calcium over Mg and phosphorus and oxalate over citrate. In plasma there was an increase in calcium and creatinine within the normal range. Calcification of tubular cells was eliminated by a preparation containing potassium, sodium and bases (from citrate degradation and bicarbonate) in addition to Mg. Less effective than the latter was Mg-potassium citrate and least effective, Mg citrate. The former treatment also normalized calcemia and urinary nitrate, but only incompletely suppressed ET-1 and had no significant effect on glomerular calcification or tissue and urinary oxalate. Urinary ET-1 excess appeared directly related to the cortical tissue calcium/Mg ratio, and urinary excretion of Mg, citrate and total protein appeared to be inversely related to the severity of C-NC. It was concluded that (1) the highly inbred rat is prone to precipitation of calcium phosphate in the renal cortex; (2) this type of C-NC occurs in close proximity to and within renal vascular tissue and is associated with an imbalance of vasoconstrictors and vasodilators of endothelial origin; (3) effective inhibition of C-NC can be achieved by an alkalinizing combination of Mg, potassium, sodium and citrate, underscoring its utility in the prophylaxis of pathological calcium phosphate deposition. The significance of these findings for the etiology and treatment of clinical disorders with renal and vascular calcification is uncertain and requires further investigation.

Alkalies↗
PubMed2002

Influence of mosapride citrate on gastric motility and autonomic nervous function: evaluation by spectral analyses of heart rate and blood pressure variabilities, and by electrogastrography.

BACKGROUND: Mosapride citrate selectively acts on serotonin (5-HT(4)) receptors, thus accelerating gastrointestinal motility via acetylcholine. However, few studies have evaluated the influence of mosapride citrate on autonomic nervous activity and hemodynamics. METHODS: The changes in autonomic nervous activity, QT interval, and QT dispersion resulting from the administration of mosapride citrate were studied. Blood pressure, electrocardiograms (ECGs), percutaneous electrogastrograms (EGGs), and ultrasonography were recorded in 20 healthy adult volunteers before and after mosapride citrate (10 mg) was administered. Autonomic nervous activity was evaluated by spectral analyses of heart rate and blood pressure variabilities. Serial changes in low-frequency components (LF, 0.04-0.15 Hz), high-frequency components (HF, 0.15-0.40 Hz), and the LF/HF ratio were investigated. RESULTS: The mean peak power of EGG increased significantly, from 86 +/- 34 microV to 131 +/- 49 microV, after the administration of mosapride citrate (P < 0.05). Gastric emptying significantly increased after the administration of mosapride citrate (P < 0.05). However, neither blood pressure nor heart rate changed significantly after the drug was administrated. In addition, spectral analyses of heart rate and blood pressure variabilities showed no significant changes in autonomic nervous activity parameters, QT intervals, or QT dispersions. CONCLUSIONS: Mosapride citrate increased gastric motility and emptying without influencing autonomic nervous activity, suggesting that it may be very useful for elderly patients or patients with autonomic imbalance.

Adult↗