Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Gluconates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources
PubMed1995

Toxicology of cupric salts in honeybees. I. Hormesis effects of organic derivatives on lethality parameters.

Feeding bees with organic cupric salts provides long-term control of the parasite Varroa jacobsoni. A set of new algebraic parameters (M. Bounias C.R. Acad. Sci. 310(3), 65-70, 1990) completely describing the population lethality function has been calculated following chronic administration of cupric gluconate, aspartate, and isoleucinate, with or without dietary pollen. Mortality curves allowed the calculation of LT50 (time for 50% lethality) as well as Hill coefficients (h) of the curves and the LD50 as a function of time. The tangent at the inflexion point of the sigmoidal time/mortality curves (delta i) gave the maximum mortality acceleration as an additional parameter. No toxicity (i.e., no decrease of TL50 vs doses and no LD50 values) was found for cupric gluconate and isoleucinate with pollen, whereas increases in LT50 and decreases in delta indicated hormesis effects. Doses decreasing by half-time LT50, h, or delta were used as objective lethality indexes for comparisons of toxicity in the other cases. Routine acute toxicity at high dosage was also compared with phosalone and lindane effects 24 hr after treatment.

Animals↗
PubMed1993

Na+ and Cl- conductances are controlled by cytosolic Cl- concentration in the intralobular duct cells of mouse mandibular glands.

Our previously published whole-cell patch-clamp studies on the cells of the intralobular (granular) ducts of the mandibular glands of male mice revealed the presence of an amiloride-sensitive Na+ conductance in the plasma membrane. In this study we demonstrate the presence also of a Cl- conductance and we show that the sizes of both conductances vary with the Cl- concentration of the fluid bathing the cytosolic surface of the plasma membrane. As the cytosolic Cl- concentration rises from 5 to 150 mmol/liter, the size of the inward Na+ current declines, the decline being half-maximal when the Cl- concentration is approximately 50 mmol/liter. In contrast, as cytosolic Cl- concentration increases, the inward Cl- current remains at a constant low level until the Cl- concentration exceeds 80 mmol/liter, when it begins to increase. Studies in which Cl- in the pipette solution was replaced by other anions indicate that the Na+ current is suppressed by intracellular Br-, Cl- and NO3- but not by intracellular I-, glutamate or gluconate. Our studies also show that the Cl- conductance allows passage of Cl- and Br- equally well, I- less well, and NO3-, glutamate and gluconate poorly, if at all. The findings with NO3- are of particular interest because they show that suppression of the Na+ current by a high intracellular concentration of a particular anion does not depend on actual passage of that anion through the Cl- conductance. In mouse granular duct cells there is, thus, a reciprocal regulation of Na+ and Cl- conductances by the cytosolic Cl- concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1994

Cell Cl and transepithelial na transport in toad urinary bladder.

Relationships between short-circuit current (Isc), cell Cl and the mechanism(s) of Cl accumulation in toad bladder epithelial cells were investigated. In serosal Cl-free gluconate Ringer, 80% of the cell Cl (measured by x-ray microanalysis) was lost over 30-60 min with an associated decrease in cell water content. concomitantly, Isc fell to 20% of its initial value within 10 min but then recovered to 45% of its initial value despite continued Cl loss. With the reintroduction of Cl, cell Cl and Isc both recovered within 10 min. Serosal SITS (4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonate; 0.5 mM) plus bumetanide (0.1 mM), did not prevent the fall in Isc or the loss of cell Cl in gluconate medium, although they did inhibit subsequent recovery of Isc in this medium. They also prevented the recovery of Isc in Cl medium but not the reaccumulation of Cl by the cells. Although SITS and bumetanide did not prevent the loss or recovery of Cl, they modified the pattern of the ion changes. In their absence, changes in cellular Cl were twice that of the changes in measured cellular cations implicating basolateral Cl/HCO3 exchange in Cl movement. With SITS plus bumetanide present, changes of similar magnitude in Cl were associated with equivalent changes in cation, consistent with the inhibition of Cl/HCO3 exchange.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1993

Synergistic activation of non-rectifying small-conductance chloride channels by forskolin and phorbol esters in cell-attached patches of the human colon carcinoma cell line HT-29cl.19A.

Cell-attached patch-clamp studies with the human colon carcinoma HT-29cl.19A cells revealed a small chloride channel with a unitary conductance of 6.5 pS at 70 mV and 4.6 pS at -70 mV clamp potential after cAMP was increased by activation of adenylyl cyclase by forskolin. Usually channels inactivated upon patch excision, but in a few excised patches the channels stayed active and displayed a linear I/V relation in symmetrical (150 mmol/l) chloride solutions with a conductance of 7.5 pS. A 16-fold increase in channel incidence was observed when forskolin and phorbol 12,13-dibutyrate (PDB) were present together. The open probability was voltage-independent and was not different in the presence of forskolin plus PDB or with forskolin alone. The conductance sequence of the channel as deduced from outward currents carried by five different anions including chloride was: Cl- > BR- > NO3- > gluconate > I-. The permeability sequence deduced from the reversal potentials was NO3- > or = Br- > Cl- > I- > gluconate. With iodide in the pipette the conductance decreased strongly. Moreover, the inward current was reduced by 61%, indicating a strong inhibition of the chloride efflux by iodide. Similarly, the forskolin-induced increase of the short-circuit current (Isc) in confluent filter-grown monolayers was strongly reduced by iodide in the apical perfusate. Iodide also increased the fractional resistance of the apical membrane and repolarized the membrane potential, indicating an inhibitory action on the forskolin-induced increase of the apical chloride conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Anions↗
PubMed1994

Whole-cell recording of the Ca(2+)-dependent slow afterhyperpolarization in hippocampal neurones: effects of internally applied anions.

Using the whole-cell recording technique, we have examined the slow Ca(2+)-activated afterhyperpolarization (AHP) and its underlying current (IAHP) in hippocampal CA1 neurones of brain slices obtained from mature rats. Specifically we have studied the effects of the anion component of various K+ salts commonly used to make the pipette filling solution that dialyses neurones during whole-cell recordings. Among the K+ salts examined which included potassium methylsulfate, potassium methanesulfonate, potassium gluconate, potassium chloride, potassium citrate and potassium glutamate, stable AHPs/IAHP and strong spike firing adaptation could only be observed in neurones recorded with the patch pipette solution containing potassium methylsulfate. These AHPs and firing patterns closely mimicked those recorded with sharp electrodes. Similarly, the sustained component of voltage-activated Ca2+ currents was more stable in neurones dialysed with cesium methanesulfonate than in those dialysed with cesium gluconate or cesium chloride. Although the mechanisms underlying the interaction(s) between internally applied anions and ionic channels need further investigation, the present experiments illustrate that in mammalian brain neurones at 33 degrees C, the Ca(2+)-activated IAHP is dramatically altered by internal anions. We suggest that among anions commonly used in electrode filling solutions for whole-cell recordings, methylsulfate is the least disruptive to intracellular structures or Ca2+ homeostasis and permits stable whole-cell recording of the IAHP and Ca2+ currents in mammalian CNS neurones.

Animals↗
PubMed1976

Oxidative phosphorylation in Micrococcus denitrificans: calculation of the P/O ratio in growing cells.

P/O ratios were measured in membrane particles obtained from cells of Micrococcus denitrificans, while growing on different carbon sources. The membrane particles obtained from cells growing actively on glucose, succinate, ethanol and propanol as the carbon and energy sources catalyzed oxidative phosphorylation and yielded respective P/O ratios of 1.4, 1.2, 0.8, and 0.5 with NADH, and 0.8, 0.6, 0.6, and 0.5 with succinate as the electron donors. Not such a difference in P/O ratio is observed in intact resting cells grown with different carbon sources. It is concluded that the influence of the carbon source is probably directed towards the efficiency of oxidative phosphorylation in membrane particles and not in the growing cells. For the aerobic carbon source-limited chemostat cultures the following maximum growth yields were determined: 40.2 and 34.2 for succinate and oxygen, 41.7 and 36.5 for malate and oxygen, 81.4 and 39.4 for mannitol and oxygen, and 77.8 and 43.4 for gluconate and oxygen respectively. With a mathematical model (de Kwaadsteniet et al., in press) the P/O ratio was valued at 1.4-1.7. YATP at mu=0.2 was valued at 8.7-10.9; YmaxATP at 9.6-13.2 and me at 0.6-4.5 for the most precise experiment (gluconate-limited). The calculation of these growth parameters has been discussed.

Aerobiosis↗
PubMed1975

Enzymatic analysis of the pathways of glucose catabolism and gluconeogenesis in Pseudomonas citronellolis.

Extracts of Pseudomonas citronellolis cells grown on glucose or gluconate possessed all the enzymes of the Entner-Doudoroff pathway. Gluconokinase and either or both 6-phosphogluconate dehydratase and KDPG aldolase were induced by growth on these substrates. Glucose and gluconate dehydrogenases and 6-phosphofructokinase were not detected. Thus catabolism of glucose proceeds via an inducible Entner-Doudoroff pathway. Metabolism of glyceraldehyde 3-phosphate apparently proceeded via glyceraldehyde 3-phosphate dehydrogenase, phosphoglycerate kinase, phosphoglycerate mutase, enolase and pyruvate kinase. These same enzymes plus triose phosphate isomerase were present in lactate-grown cells indicating that synthesis of triose phosphates from gluconeogenic substrates also occurs via this pathway. Extracts of lactate grown-cells possessed fructose diphosphatase and phosphohexoisomerase but apparently lacked fructose diphosphate aldolase thus indicating either the presence of an aldolase with unusual properties or requirements or an alternative pathway for the conversion of triose phosphate to fructose disphosphate. Cells contained two species of glyceraldehyde 3-phosphate dehydrogenase, one an NAD-dependent enzyme which predominated when the organism was grown on glycolytic substrates and the other, an NADP-dependent enzyme which predominated when the organism was grown on gluconeogenic substrates.

Fructose-Bisphosphatase↗
PubMed1976

Glycolysis and glycogen metabolism after inhibition of hexose monophosphate pathway in C6-GLIAL cells.

1. 6-Aminonicotinamide (0.01 mg/ml) leads to a strong accumulation of 6-PG in C6 glial cells after 24h. 2. The accumulated 6-PG is dephosphorylated to gluconate which easily permeates the cell membrane. Extracellular gluconate is formed at a rate of 12% of the total glucose consumption. 3. 6-PG as competitive inhibitor of the PG1 caused a reduction of the glycolytic flux of about 40%. 4. The reduced glycolytic flux lowers the ATP concentration under anaerobic conditions to 75% of the controls. 5. The glycogen content after 6-AN is increased by 50%, probably by the activation of the glycogen synthetase due to the higher Glc 6-P concentration. 6. The fibroblast-like morphology of the C6 cell line has typically changed under 6-aminonicotinamide.

6-Aminonicotinamide↗
PubMed1977

Glucose metabolism in C-1300 neuroblastoma cells after inhibition of hexose monophosphate pathway.

1. Application of 6-AN (0.01 mg/ml) leads to a strong accumulation of 6-PG in C-1300 neuroblastoma cells which, however, only amounts to one third of that found in C-6 glial cells. 2. In C-1300 neuroblastoma cells dephosphorylation of the accumulated 6-PG causes a rise of the intracellular gluconate to eight times the value found for 6-PG. It is four times higher than the gluconate content observed in C-6 glial cells. 3. Although 6-PG is a competitive inhibitor of PGI it causes no reduction of glycolytic flux and ATP content in stationary phase C-1300 neuroblastoma cells in contrast to the strong reduction of glycolytic flux and ATP content observed in C-glial cells. 4. The intracellular Glc-6-P and Fru-6-P content of C-1300 neuroblastoma cells increases by four to five times after treatment with 6-AN. Both this increase and the decrease of Fru-1,6-P2 content point to an inhibition of the phosphofructokinase. 5. In contrast to C-6 glial cells no morphological changes could be observed in C-1300 neuroblastoma cells up to 24 h after administration of 6-AN.

6-Aminonicotinamide↗
PubMed1987

Intracellular pH in the rat mandibular salivary gland: the role of Na-H and Cl-HCO3 antiports in secretion.

Intracellular pH (pHi) in the perfused rat mandibular gland was determined from the distribution of DMO (5,5-dimethyl-2,4-oxazolidinedione). In unstimulated glands, pHi averaged 7.12 +/- 0.02. Stimulation with a "standard" (submaximal) concentration (0.3 mumol/l) of acetylcholine (ACh) caused a fall in pHi to 6.81 +/- 0.06 over 60 min, but a maximal concentration (1.0 mumol/l) caused an initial rise in pHi to 7.60 +/- 0.02, followed by a fall to 7.45 +/- 0.02 over 60 min. After replacement of perfusate Cl with gluconate, the standard ACh concentration caused a rise in pHi to 7.50 +/- 0.02 followed by a fall to 7.27 +/- 0.04 after 60 min, concomitant with a 76% fall in secretory rate and a rise in salivary HCO3 concentration from 14 +/- 0.9 to 67 +/- 1.5 mmol/l. Furosemide (1 mmol/l) had a similar effect to gluconate replacement except that secretory rate fell only by 60%. Bumetanide (1 mmol/l), which inhibited secretion by 67%, did not cause pHi to rise following ACh stimulation but prevented the fall seen with ACh alone. Acetazolamide and methazolamide (1 mmol/l) had no effect on the salivary secretory response to ACh but they caused pHi to rise, respectively, to 7.20 +/- 0.03 and 7.43 +/- 0.02. Bumetanide and methazolamide together caused pHi to rise to 7.58 +/- 0.02 and reduced the secretory response to ACh by 91%. The disulfonic stilbene, SITS, caused pHi to rise to 7.26 +/- 0.03. Ouabain and amiloride both caused resting pHi to fall closer to equilibrium and largely abolished the gland's responsiveness to ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Interdependence of H+ and K+ fluxes during the Ca(2+)-pumping activity of sarcoplasmic reticulum vesicles.

The release of H+ during the oxalate-supported Ca2+ uptake in sarcoplasmic reticulum vesicles is kinetically coincident with the initial phase of Ca2+ accumulation. The Ca2+ uptake is increased and the H+ release is decreased in the presence of KCl and other monovalent chloride salts as expected for a H(+)-monovalent cation exchange. The functioning of the Ca(2+)-pump is disturbed by the presence of potassium gluconate and to a lesser extent, of choline chloride. These salts do not inhibit the ATPase activity of Ca(2+)-permeable vesicles, suggesting a charge imbalance inhibition which is specially relevant in the case of gluconate. Therefore, K+, and also Cl-, appear to be involved in secondary fluxes during the active accumulation of Ca2+. The microsomal preparation seems homogeneous with respect to the K(+)-channel, showing an apparent rate constant for K+ release of approximately 25 s-1 measured with the aid of 86Rb+ tracer under equilibrium conditions. A Rb+ efflux, sensitive to Ca(2+)-ionophore, can be also detected during the active accumulation of Ca2+. The experimental data suggest that both monovalent cations and anions are involved in a charge compensation during the Ca2+ uptake and H+ release. Fluxes of these highly permeable ions would contribute to cancel the formation of a resting membrane potential through the sarcoplasmic reticulum membrane.

Animals↗
PubMed1988

Biliary calcium and bile acid secretion in intact and TPTX rats with varying plasma calcium concentration.

Investigations of the effects of plasma calcium concentration on the relationship between biliary secretion of bile acid and calcium were performed in normocalcemic, calcium gluconate-induced hypercalcemic, thyroparathyroidectomy-induced hypocalcemic (TPTX) rats, and TPTX rats that received calcium gluconate to maintain normocalcemia. Studies were done at normal bile flow and at sodium taurocholate-stimulated bile flow. The results showed that biliary calcium secretion, which could occur in the absence of parathyroid hormone and calcitonin, was dependent mainly on plasma calcium concentration and was only partly influenced by bile acid secretion. Concerning the route of biliary calcium secretion, 80% was by the transcellular pathway and 20% was by the paracellular pathway. During theophylline-stimulated bile-acid-independent bile flow, the increase in bile-acid-independent calcium was found to be secreted by both pathways.

Animals↗
PubMed1988

Apical Na+ permeability of frog skin during serosal Cl- replacement.

Gluconate substitution for serosal Cl- reduces the transepithelial short-circuit current (Isc) and depolarizes short-circuited frog skins. These effects could result either from inhibition of basolateral K+ conductance, or from two actions to inhibit both apical Na+ permeability (PapNa) and basolateral pump activity. We have addressed this question by studying whole-and split-thickness frog skins. Intracellular Na+ concentration (CcNa) and PapNa have been monitored by measuring the current-voltage relationship for apical Na+ entry. This analysis was conducted by applying trains of voltage pulses, with pulse durations of 16 to 32 msec. Estimates of PapNa and CcNa were not detectably dependent on pulse duration over the range 16 to 80 msec. Serosal Cl- replacement uniformly depolarized short-circuited tissues. The depolarization was associated with inhibition of Isc across each split skin, but only occasionally across the whole-thickness preparations. This difference may reflect the better ionic exchange between the bulk medium and the extracellular fluid in contact with the basolateral membranes, following removal of the underlying dermis in the split-skin preparations. PapNa was either unchanged or increased, and CcNa either unchanged or reduced after the anionic replacement. These data are incompatible with the concept that serosal Cl- replacement inhibits PapNa and Na,K-pump activity. Gluconate substitution likely reduces cell volume, triggering inhibition of the basolateral K+ channels, consistent with the data and conclusions of S.A. Lewis, A.G. Butt, M.J. Bowler, J.P. Leader and A.D.C. Macknight (J. Membrane Biol. 83:119-137, 1985) for toad bladder. The resulting depolarization reduces the electrical force favoring apical Na+ entry. The volume-conductance coupling serves to conserve volume by reducing K+ solute loss. Its molecular basis remains to be identified.

Animals↗
PubMedDate not supplied

In vitro influence of zinc and magnesium on the deformability of red blood cells artificially hardened by heating.

Trace elements have been shown to improve red blood cell (RBC) deformability: zinc in sickle cell disease and magnesium in an in vitro model of chemically rigidified erythrocytes. In this study, we investigated the effect and the influence of incubation time of zinc or magnesium on an in vitro model of rigidified RBCs by heating. Erythrocyte rigidity was determined by viscosimetry at high shear rate by a falling ball viscosimeter MT 90. In the first part of the study, six normal volunteers participated. Viscosimetry was performed on native blood before and after heating the sample for 10 min at 50 degrees C. Therefore, increasing concentrations of zinc gluconate (final concentration: 0.5-4 g/L) or isotonic NaCl as control medium were added to the sample. Heating induced a twofold increase in all indices of RBC rigidity (p < 0.05). At all these concentrations of zinc, a highly significant, dose-related fluidifying effect was observed (40-70%): this effect was immediately obtained and did not change over 60 min. Even at the highest concentration, recovery was not complete. In the second part of the study, we studied magnesium's effects on blood. In a first protocol, whole blood was rigidified by heating at 56 degrees C for 10 min, and the correcting effect of 5 min of incubation at 37 degrees C of RBCs in 150 mmol/L NaCl, MgSO4, magnesium acetate, and magnesium gluconate was investigated. In a second protocol, the same incubation with NaCl and magnesium salts was made on blood that had not been previously heated.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed2005

[Pancytopenia, arthralgia and myeloneuropathy due to copper deficiency].

BACKGROUND: Copper deficiency leads to hematologic disorders like pancytopenia. In addition, myeloneuropathy was described in a few cases reports. CASE REPORT: A 71-year-old woman was hospitalized because of increasing pancytopenia and ataxic gait, that resulted in a near-complete inability to walk without assistance. Additional symptoms included arthralgia, reduced appetite and weight loss. Laboratory studies revealed a proteinuria of 3,700 mg/day. Magnetic resonance imaging of the cervical and thoracic spine revealed a wedge-shaped signal intensity in the dorsal part as a sign of damage in this area. A copper deficiency was then identified as the likely underlying cause for the low blood cell counts and neurologic deficits. In this patient, the copper deficiency may have resulted from a disturbance in absorption due to a partial gastrectomy (modified Billroth I) 10 years ago and due to urinary copper loss in view of mesangioproliferative glomerulonephritis. A therapy with copper gluconate 3 x 3 mg/day was initiated. Within 2 weeks, blood cell counts normalized and appetite became normal again; just so, arthralgia disappeared. The neurologic symptoms persisted, even though the copper substitution continued for 6 months. CONCLUSION: Copper deficiency may be a differential diagnosis for hematologic abnormalities like pancytopenia, even if a disorder of intestinal resorption or a proteinuria occurs. Myeloneuropathy is a rare complication of this deficiency. Hemograms may become normal after treatment with oral copper gluconate, but at least in the case presented here, neurologic symptomes did not show any improvement.

Aged↗
PubMed2004

Characterisation of a secondary alcohol dehydrogenase from Xanthomonas campestris DSM 3586.

The chromosomal locus NP_636946 of Xanthomonas campestris DSM 3586 (ATCC 33913) which was earlier presumed to encode a quinoprotein glucose dehydrogenase has been cloned, expressed in Escherichia coli and the recombinant enzyme has been characterised. It was found to have no glucose dehydrogenase activity but to be active on many different polyols and diols, aliphatic alcohols, certain aldonic acids and amino-sugars. The product of D: -gluconic acid oxidation was 5-keto-D: -gluconic acid. The enzyme differs from polyol/gluconate dehydrogenases found in Gluconobacter by its single-chain architecture, different substrate specificity and much higher (20- to 30-fold) expression level in E.coli.

Alcohol Oxidoreductases↗
PubMed2001

Production of glucose-fructose oxidoreductase and ethanol by Zymomonas mobilis ATCC 29191 in medium containing corn steep liquor as a source of vitamins.

Different concentrations of corn steep liquor (CSL) were tested in the cultivation of Zymomonas mobilis. Cell growth, ethanol production, and the formation of glucose-fructose oxidoreductase (GFOR) and glucono-delta-lactonase (GL), the enzymes responsible for the bio-production of gluconic acid and sorbitol, were examined. The cell yields using 25 g CSL l(-1) and 40 g CSL l(-1) (Y(X,S) approximately 0.031 g g(-1)) were close to that obtained with 5 g yeast extract (YE) l(-1). With 5 g CSL l(-1) and 15 g CSL l(-1), the nutritional limitation led to smaller Y(X/S). Using 100 g CSL l(-1) produced an inhibitory effect on cell growth. Similar ethanol yields (92-95%) were calculated for each concentration of CSL and also for YE medium. The highest specific GFOR/GL activities (13.2-13.5 U g(-1) dry cell) were reached with 25 g CSL l(-1) and 40 g CSL l(-1), values comparable to that achieved with 5 g YE l(-1). The results confirm that CSL is an effective and cheap supplement for Z. mobilis medium, increasing the economic potential of a large-scale bio-production of sorbitol and gluconic acid by untreated Z. mobilis cells. The economic feasibility of the process is discussed.

Culture Media↗
PubMedDate not supplied

Modified intra-arterial calcium stimulation with venous sampling test for preoperative localization of insulinomas.

BACKGROUND: To determine the accuracy and safety of a modified intra-arterial calcium stimulation with the venous sampling test (ASVS) for preoperative localization of insulinomas. Modification included stimulation with a fixed low dose of calcium gluconate, additional stimulation in the distal splenic artery, and no insulin sampling in the left hepatic vein. METHODS: In 10 patients showing biochemical evidence of organic hyperinsulinemia, 0.45 mmol of Ca2+ was injected into the gastroduodenal, superior mesenteric, proper hepatic, proximal, and distal splenic arteries during angiography. Insulin levels were measured in samples taken from the right hepatic vein before and 30, 60, 90, 120, 180, and 300 s after Ca2+ injection. RESULTS: Insulin gradients with an increase of more than fourfold indicated direct tumor supply, two- to fourfold correlated with collateral supply, and less than twofold correlated with normal tissue vascularization. ASVS localized all the adenomas of the pancreatic head (n = 3) and body (n = 2) and two of four adenomas of the tail correctly, as confirmed by surgery. Two adenomas of the proximal pancreatic tail were erroneously localized to the body segment, but the fault was rectified by angiography. In one patient with a negative ASVS and without exploration, the diagnosis of an insulinoma was revised. CONCLUSION: ASVS with a fixed low dose of calcium gluconate is a highly accurate and safe method for preoperative localization of insulinomas. Sampling in the left hepatic vein can be routinely omitted. Additional stimulation in the distal splenic artery seems helpful in surgical decision making, but additional experience is needed.

Adult↗