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PubMed2002

Localization of gastrinomas by selective intra-arterial calcium injection.

BACKGROUND: Preoperative localisation is important for successful surgical treatment of gastrinomas. However, a satisfactory method that achieves this has not been defined, and at present somatostatin receptor scintigraphy and selective intra-arterial stimulation testing with secretin have the greatest sensitivities. As secretin is now difficult to obtain, we decided to explore the use of calcium gluconate as a secretagogue. High extracellular calcium concentrations cause degranulation of neuroendocrine cells and subsequent release of hormone. METHODS: Two patients with biochemically proven gastrinomas were investigated pre-operatively. Under angiographic control calcium gluconate was injected into the arteries supplying the pancreas and duodenum, gastrin levels were then determined in hepatic vein samples obtained before and 30, 60, 90, 120 and 180 seconds after each injection. One of the patients had also previously undergone selective intra-arterial stimulation testing with secretin. RESULTS: Calcium gluconate produced sharp peaks of gastrin which unequivocally localised the tumour to a specific vascular territory in each case. Furthermore, surgery confirmed the localisations of the gastrinomas. Calcium injection, unlike secretin, into vascular territories without gastrinomas caused no rise in gastrin, thereby demonstrating calcium's greater specificity. CONCLUSIONS: Calcium gluconate is a highly sensitive and specific alternative secretagogue to secretin for localisation of pancreatic and duodenal gastrinomas. Furthermore calcium gluconate was found to demonstrate the territory of the tumour more accurately than secretin.

Adult↗
PubMed1998

Comparative study of the in vitro inflammatory activity of three nickel salts on keratinocytes.

Nickel, the allergen of contact dermatitis, induces the in vitro production of inflammation markers such as intracellular adhesion molecule-1, interleukin-1 and tumour necrosis factor-alpha by keratinocytes. The purpose of our study was to compare the effect in vitro of different nickel salts on keratinocyte activation in order to determine whether this process depends on the nature of the salt used. Cultured keratinocytes were incubated with three nickel salts for 24 h in MCDB153 medium without hydrocortisone. Nickel gluconate, nickel sulphate and nickel chloride were each used at four concentrations: 5.10(-5) M, 1.10(-4) M and 1.10 (-3) M. Keratinocyte activation was studied through the production of three inflammation markers: intracellular adhesion molecule-1, tumour necrosis factor-alpha and very late antigen-3 (an integrin with increased expression during contact dermatitis). Marker production was detected by immunocytochemistry and flow cytometry. Tumour necrosis factor-alpha production and intracellular adhesion molecule-1 and very late antigen-3 expression increased with addition of the three nickel salts, becoming maximal for nickel gluconate 1.10(-4) M. In a subsequent experiment, zinc gluconate (an anti-inflammatory molecule) at 9 micrograms/ml reduced the very late antigen-3 expression induced by nickel gluconate 1.10(-4) M. Therefore, this study enabled us to determine the concentration of a nickel salt (nickel gluconate) inducing optimal keratinocyte activation in our culture conditions and also indicated the potential interest of very late antigen-3 as an inflammation marker.

Anti-Inflammatory Agents↗
PubMedDate not supplied

A study to determine the efficacy of treatments for hydrofluoric acid burns.

Hydrofluoric acid burns are characterized by progressive tissue destruction and severe pain. Fluoride ion chelators, such as salts of calcium and magnesium, have been used to treat these burns. This study was designed to compare the efficacy of several treatment methods that involve the use of these salts. Standard hydrofluoric acid burns were produced on the shaved hindquarters of rats. After being rinsed with water, the chemical burns were treated by one of seven experimental methods. The progress of the chemical burn damage was observed for 1 week by measuring the surface areas of the burns. Calcium gluconate burn jelly, 20% calcium gluconate in water, and 50% aqueous dimethyl sulfoxide did not significantly slow the spread of the burn area. However, subcutaneous injections of calcium gluconate or magnesium sulfate and topical applications of calcium gluconate in a solution of dimethyl sulfoxide significantly slowed the progress of the burns during the first 24 hours and enhanced tissue recovery for the remainder of the observation period. These results indicate that subcutaneous injections of magnesium or calcium salts appear to be more effective than conventional topical applications in the treatment of hydrofluoric acid burns. More significantly, topically applied calcium gluconate combined with a penetration enhancer, such as dimethyl sulfoxide, is as effective as injection treatments in reducing damage caused by hydrofluoric acid.

Administration, Topical↗
PubMed1994

The effect of intracellular anions on ATP-dependent potassium channels of rat skeletal muscle.

1. We have used excised inside-out patches to study the effects of anions bathing the cytoplasmic surface of the membrane on ATP-dependent K+ channels of rat flexor digitorum brevis muscle. Channels were closed by ATP applied to the cytoplasmic face of the patch with a concentration for half-closure (Ki) of 14 microM, were highly selective for K+ and had unitary conductances of 62 pS in symmetrical 155 mM K+ and 27 pS in 5 mM [K+]o. 2. In 139 mM Cl- internal solution channel activity declined rapidly after excision of the patch. Inclusion of 40 mM potassium gluconate (substituted for KCl) in the solution both restored channel activity and greatly slowed its subsequent run-down. 3. The action of gluconate was concentration dependent. The effect did not involve a change in ATP binding, since the Ki for ATP was not significantly changed by gluconate, and was specific for the cytoplasmic face of the patch. 4. The anions pyruvate, lactate and acetate were all able to restore channel activity after run-down, though less well than gluconate, while sulphate and methylsulphate were without effect. 5. Analysis of single channel kinetics showed that gluconate did not affect mean open lifetime, but led to a decrease in the number and duration of long closings. 6. Anions are most likely to act by stabilizing the structure of the channel protein. Changes in the intracellular concentration of certain anions may play a role in regulating channel activity.

Adenosine Triphosphate↗
PubMed1982

Detection of glucose oxidation products in chilled fresh beef undergoing spoilage.

The fate of nutrients during storage of longissimus dorsi muscle at 4 degrees C was examined. Glucose concentrations in meat were shown to decrease concomitantly with an approximately fourfold increase in the activity of glucose dehydrogenase. Gluconate concentrations in meat were determined by an enzyme assay and shown to increase from 2.1 to 40.6 microgram/g upon storage of the meat from day 0 to day 6. At day 12, gluconate concentrations had decreased to 5.8 microgram/g. Dark firm dry meat, which contains little or no glucose, did not exhibit the same rise and fall in gluconate concentration. Thin-layer chromatographic analysis confirmed the presence of 2-ketogluconate in 6- and 12-day-old longissimus dorsi muscle that had been stored at 4 degrees C. Gluconate concentrations in irradiated sterile meat inoculated with Pseudomonas fluorescens increased from 4.2 to 77.8 microgram/g during the first 6 days of storage at 4 degrees C. Therefore, glucose in meat stored at 4 degrees C appeared to be converted to gluconate, 2-ketogluconate, or both extracellularly by one of the main meat spoilage organisms, most likely the pseudomonads.

Animals↗
PubMed1995

Cloning of a mineral phosphate-solubilizing gene from Pseudomonas cepacia.

We have recently shown that the ability of some gram-negative bacteria to dissolve poorly soluble calcium phosphates (Mps+ phenotype) is the result of periplasmic oxidation of glucose to gluconic acid via the quinoprotein glucose dehydrogenase (GDH), a component of the direct oxidation pathway. Escherichia coli K-12 derivatives synthesize apo-GDH but not the cofactor pyrroloquinoline-quinone (PQQ) essential for formation of the holoenzyme. Therefore, in the absence of exogenous PQQ, these strains do not produce gluconic acid and are Mps-. Evidence is presented to show that expression of a single 396-base Pseudomonas cepacia open reading frame (designated gabY) in E. coli JM109 (a K-12 derivative) was sufficient to induce the Mps+ phenotype and production of gluconic acid. We present the nucleotide sequence of this open reading frame which coded for a protein (GabY) with a deduced M(r) of 14,235. Coupled transcription-translation of a plasmid (pSLY4 or pGAB1) carrying gabY resulted in production of a protein with an M(r) of 14,750. Disruption of the open reading frame of gabY via site-directed mutagenesis changed the phenotype to Mps- and eliminated gluconic acid production. The deduced amino acid sequence of gabY has no apparent homology with those of previously cloned direct oxidation pathway genes but does share regions highly homologous with the histidine permease system membrane-bound protein HisQ as well as other proteins in this family. In the presence of 1 microM exogenous PQQ, both JM109(pSLY4) and JM109(pGAB1) produced 10 times as much gluconic acid as was seen with either the plasmid or exogenous PQQ alone.(ABSTRACT TRUNCATED AT 250 WORDS)

ATP-Binding Cassette Transporters↗
PubMed1971

2-keto-3-deoxygluconate 6-phosphate aldolase mutants of Escherichia coli.

A new mutation in Escherichia coli, giving inability to grow on gluconic, glucuronic, or galacturonic acids, has been identified as complete deficiency of 2-keto-3-deoxygluconate 6-phosphate (KDGP) aldolase activity. The genetic map position of the locus, eda, is about 35 min. The inability to grow on the uronic acids was expected, because the aldolase is on the sole known pathway of their metabolism. However, inability to grow on gluconate was less expected, because the hexose monophosphate shunt might be used, as happens in mutants blocked in the previous step, edd, of the Entner-Doudoroff pathway. The likely explanation of gluconate negativity is inhibition by accumulated KDGP, because gluconate is inhibitory to growth on other substances, and one type of gluconate revertant is eda(-), edd(-). KDGP is probably the inducer of KDGP aldolase.

Alcohol Oxidoreductases↗
PubMed1982

Pseudomonas cepacia mutants blocked in the Entner-Doudoroff pathway.

Pseudomonas cepacia mutants deficient in either 6-phosphogluconate (6PGA) dehydratase (Edd-) or 2-keto-3-deoxy-6-phosphogluconate (KDPG) aldolase (Eda-) failed to utilize glucose or gluconate despite the prominence of of 6-phosphogluconate dehydrogenase (6PGAD) ii this bacterium and the potential for utilizing the pentose shunt suggested by its growth on ribitol and xylose. The Eda- strains grew normally on glucuronic acid, indicating that in P. cepacia its degradation does not depend upon KDPG aldolase as it does in Escherichia coli. Both 6PGA dehydratase and KDPG aldolase were inducible enzymes, with 6PGA rather than gluconate the apparent inducer. Edd- as well as Eda- strains were sensitive to growth inhibition by glucose, gluconate, fructose, and related carbohydrates when these substrates were present in combination with alternate carbon sources such as citrate or phthalate, presumably as a consequence of accumulation and toxicity of 6PGA, KDPG, or both. Edd- mutants were somewhat less sensitive to such inhibition than were Eda- strains. Certain derivatives of the Edd- strains we examined were able to utilize gluconate despite their deficiency of 6PGA dehydratase. Such mutants formed higher levels of 6PGAD than did the wild type. It is likely that the elevated levels of 6PGAD in these strains prevents accumulation of toxic levels of 6PGA that would otherwise result from a block in he Entner-Doudoroff pathway. The results suggest that P. cepacia can mutate to grow slowly on gluconate utilizing only the pentose shunt.

Aldehyde-Lyases↗
PubMed1983

Regulation of alternate peripheral pathways of glucose catabolism during aerobic and anaerobic growth of Pseudomonas aeruginosa.

Glucose may be converted to 6-phosphogluconate by alternate pathways in Pseudomonas aeruginosa. Glucose is phosphorylated to glucose-6-phosphate, which is oxidized to 6-phosphogluconate during anaerobic growth when nitrate is used as respiratory electron acceptor. Mutant cells lacking glucose-6-phosphate dehydrogenase are unable to catabolize glucose under these conditions. The mutant cells utilize glucose as effectively as do wild-type cells in the presence of oxygen; under these conditions, glucose is utilized via direct oxidation to gluconate, which is converted to 6-phosphogluconate. The membrane-associated glucose dehydrogenase activity was not formed during anaerobic growth with glucose. Gluconate, the product of the enzyme, appeared to be the inducer of the gluconate transport system, gluconokinase, and membrane-associated gluconate dehydrogenase. 6-Phosphogluconate is probably the physiological inducer of glucokinase, glucose-6-phosphate dehydrogenase, and the dehydratase and aldolase of the Entner-Doudoroff pathway. Nitrate-linked respiration is required for the anaerobic uptake of glucose and gluconate by independently regulated transport systems in cells grown under denitrifying conditions.

Aerobiosis↗
PubMed2000

Zinc salts inactivate clinical isolates of herpes simplex virus in vitro.

Using a standard plaque assay and clinical isolates of herpes simplex virus (HSV), we have tested the ability of zinc salts to inactivate HSV. Virus was treated by incubation at 37 degrees C with zinc salts in morpholinepropanesulfonic acid-buffered culture medium and was then diluted and plated onto CV-1 cells for detection and quantitation of remaining infectious virus. Of 10 randomly chosen clinical isolates (five HSV type 1 [HSV-1] isolates and five HSV-2 isolates), seven were inactivated >98% by treatment in vitro with 50 mM zinc gluconate for 2 h and nine were inactivated >97% by treatment with zinc lactate. The effect was concentration dependent. With an HSV-1 isolate, 50 mM zinc gluconate or zinc lactate caused 100% inactivation, 15 mM caused 98 to 99% inactivation, and 5 mM caused 63 to 86% inactivation. With an HSV-2 isolate, 50 and 15 mM zinc gluconate caused 30% inactivation and 5 and 1 mM caused less than 9% inactivation, whereas 50 and 15 mM zinc lactate caused greater than 92% inactivation and 5 and 1 mM caused 37 and 26% inactivation, respectively. The ability of the zinc salts to inactivate HSV was not related to pH in the pH range of 6.1 to 7.6 since inactivation by zinc gluconate or zinc lactate in that pH range was 99.7 to 100% with a 2-h treatment with 50 mM zinc salt. Short (5-min) treatments of selected isolates with zinc gluconate, zinc lactate, zinc acetate, or zinc sulfate yielded inactivation rates of 0 to 55%.

Adult↗
PubMed1977

Effects of calcium on renin and aldosterone in the rat.

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.

Adrenal Glands↗
PubMedDate not supplied

Effects of impermeant medium ions on the composition of rabbit renal cortical slices.

When incubated in isosmotic oxygenated medium in which chloride was completely replaced by gluconate, rabbit renal cortical slices lost chloride with sodium, potassium and water before reaching a new steady-state composition after 15-30 min. When corrected for extracellular space, there was an electroneutral loss of alkali metal cations (Na + K) with chloride, accompanied by isosmotic loss of water from the cells. The losses of chloride and water were independent of medium pH over the range of 6.4-8.2, and were the same with potassium rather than sodium as the dominant medium cation. Incubation in isosmotic sodium chloride medium restored tissue composition of slices transferred from gluconate medium. This recovery was not dependent specifically upon medium chloride, for slice water content also recovered when nitrate rather than chloride was substituted for medium gluconate. With sodium completely replaced by n-methyl d-glucamine (nmdG+), cells in slices lost far more sodium and potassium than chloride before reaching a new steady-state composition after some 30 min. However, the loss of water was as predicted from the total losses of measured inorganic ions. With sodium and chloride completely replaced by nmdG+ and gluconate, there was a greater loss of water than found with unilateral substitutions. Again, the combined loss of diffusible inorganic cations exceeded the loss of chloride but the water loss was that expected for isosmotic loss accompanying the measured losses of ions. These results reveal that both gluconate and nmdG+ behave as impermeant ions in this tissue preparation. It is suggested that, in the absence of medium sodium, sodium-hydrogen exchange is inhibited. Retained hydrogen ions are buffered on charged cellular non-diffusible solutes and the associated hydroxyl (or bicarbonate) ions are lost from the cells accompanied by the inorganic univalent cations lost in excess of chloride in nmdG+ medium.

Animals↗
PubMed1988

Purification and characterization of a repressor for the Bacillus subtilis gnt operon.

The GntR protein is a negative regulator involved in gluconate-inducible expression of the Bacillus subtilis gnt operon which is responsible for gluconate metabolism. The GntR protein has been purified to homogeneity from an overproducing Escherichia coli strain harboring a gntR gene-carrying plasmid. The total amino acid composition and the NH2-terminal amino acid sequence of the purified protein were essentially the same as those deduced from the nucleotide sequence of the gntR gene. Molecular weight determination by gel filtration revealed that the purified protein is in a highly polymerized form, but it likely exists as a dimer when highly diluted. The purified GntR protein was found to be specifically bound to DNA fragments carrying the promoter of the gnt operon in an electrophoretic mobility shift assay. This binding was specifically inhibited by the addition of gluconate or glucono-delta-lactone. The purified protein repressed in vitro transcription from the promoter of the gnt operon. This repression was suppressed by gluconate or glucono-delta-lactone. These results indicate that the GntR protein is a repressor for the gnt operon and that gluconate and glucono-delta-lactone are inducers for this operon.

Bacillus subtilis↗
PubMed1990

Effect of propentofylline on the biochemical lesion of the rat brain in aluminium-induced neurotoxicity.

Acute and chronic administration of Al-gluconate (12.7% Al) at the concentration of 1 mg/kg produces edema in the rat brain, as reflected by the increase in water and Na+ content. The permeability for Evans blue is also increased, which indicates the opening of the blood-brain barrier. Higher concentrations of the Al-gluconate (10 mg/kg) change, in acute experiments, the pattern of energy metabolites in the rat brain toward a profile observed in a deep hypoxia. Chronic administration of a low concentration of Al-gluconate (1 mg/kg) increases the local utilization of glucose in 20 of 39 rat brain structures examined. This increase was particularly evident in the structures of the limbic system. Xanthine derivative propentofylline reverses the edema formation in acute and chronic experiments. Hypoxia-like changes in energy metabolism are also reversed by propentofylline. In preliminary experiments propentofylline also suppressed the increased utilization of glucose observed after administration of Al-gluconate. These results suggest that (i) the Al-gluconate model in rats can be used to study Al-neurotoxicity at a very low level of Al, and (ii) the xanthine derivative propentofylline can eventually be used to abolish the Al-neurotoxicity.

Adenosine Triphosphate↗
PubMed1998

The cation selectivity of the sarcoball Ca2+ channel in frog muscle fibres.

We have measured single-channel currents from sarcoplasmic reticulum (SR) blebs (sarcoballs) of frog skeletal muscle fibres using conventional patch-clamp electrodes with excised patches. With both the pipette and bath solutions containing 50 mM Ca(gluconate)2 the slope conductance of the single channels was 39.2 pS for the most commonly seen state, with a reversal potential of -0.4 mV. The cation selectivity of this channel was investigated by replacing the bathing solution with either gluconate or HEPES salts of selected cations. The Goldman permeability ratios, calculated from the reversal potentials, were found to be P(Ca2+)/P(K+)=2.4, P(Ca2+)/ P(Na+)=2.7, P(Ca2+)/P(Tris+)=3.1, P(Ca2+)/P(Mg2+)=1.0 and P(Ca2+)/P(Ba2+)=1.1. Each value for the monovalent ions was found to be less than the corresponding value reported for the SR ryanodine receptor channel from skeletal and cardiac muscle. Single-channel activity could be recorded when the preparation was bathed in symmetrical 50 mM Mg(gluconate)2 solutions, and these channels had a similar conductance and open probability to that measured when the preparation was bathed in symmetrical Ca(gluconate)2 solution. The channel activity in symmetrical 50 mM Ca(gluconate)2 solution was insensitive to bath-applied caffeine (5 mM) and ryanodine (10 microM). The results are in agreement with the conclusion that the sarcoball Ca2+ channel is not the ryanodine receptor release channel, but possibly a form of the SR Ca2+-ATPase which is uncoupled from the catalytic events of the pump and acts as a passive ion channel.

Animals↗
PubMed1988

Modulation of ATP-dependent Ca2+ transport in rat parotid basolateral membrane vesicles by K+ + Cl- flux.

In basolateral membrane vesicles (BLMV) isolated from rat parotid glands, the initial rate of ATP-dependent Ca2+ transport, in the presence of KCl, was approx. 2-fold higher than that obtained with mannitol, sucrose or N-methyl-D-glucamine (NMDG)-gluconate. Only NH4+, Rb+, or Br- could effectively substitute for K+ or Cl-, respectively. This KCl activation was concentration dependent, with maximal response by 50 mM KCl. An inwardly directed KCl gradient up to 50 mM KCl had no effect on Ca2+ transport, while equilibration of the vesicles with KCl (greater than 100 mM) increased transport 15-20%. In presence of Cl-, 86Rb+ uptake was 2.5-fold greater than in the presence of gluconate. 0.5 mM furosemide inhibited 86Rb+ flux by approx. 60% in a Cl- medium and by approx. 20% in a gluconate medium. Furosemide also inhibited KCl activation of Ca2+ transport with half maximal inhibition either at 0.4 mM or 0.05 mM, depending on whether 45Ca2+ transport was measured with KCl (150 mM) equilibrium or KCl (150 mM) gradient. In a mannitol containing assay medium, potassium gluconate loaded vesicles had a higher (approx. 25%) rate of Ca2+ transport than mannitol loaded vesicles. Addition of valinomycin (5 microM) to potassium gluconate loaded vesicles further stimulated (approx. 30%) the Ca2+ transport rate. These results suggest that during ATP dependent Ca2+ transport in parotid BLMV, K+ can be recycled by the concerted activities of a K+ and Cl- coupled flux and a K+ conductance.

Adenosine Triphosphate↗
PubMed2006

Solid-liquid distribution of selected concrete admixtures in hardened cement pastes.

The distribution between hardened cement paste and cement pore water of selected concrete admixtures (BZMs), i.e., sulfonated naphthalene-formaldehyde condensate (NS), lignosulfonate (LS) and a gluconate-containing plasticiser used at the Paul Scherrer Institute for waste conditioning, was measured. Sorption data were fitted to a single-site Langmuir isotherm with affinity constants K=(19+/-4)dm(3)g(-1) for NS, K=(2.1+/-0.6) dm(3)g(-1) for LS and sorption capacities q=(81+/-16)g kg(-1) for NS, q=(43+/-8)g kg(-1) for LS. In the case of gluconate, a two-site Langmuir sorption model was necessary to fit the data satisfactorily. Sorption parameters for gluconate were K(1)=(2+/-1)x10(6)dm(3)mol(-1) and q(1)=(0.04+/-0.02)mol kg(-1) for the stronger binding site and K(2)=(2.6+/-1.1)x10(3)dm(3)mol(-1) and q(2)=(0.7+/-0.3)mol kg(-1) for the weaker binding site. Desorption of these BZMs from cement pastes and pore water in cement specimens prepared in the presence of the BZMs were then used to test the model. It was found that only minor parts of NS and LS could be mobilised as long as the cement composition was intact, whereas the sorption of gluconate was found to be reversible. The Langmuir model makes valuable predictions in the qualitative sense in that the pore water concentration of the BZMs is reduced by several orders of magnitude as compared to the initial concentrations. In view of the necessity for conservative predictions used in the safety analysis for disposal of radioactive waste, however, the predictions are unsatisfactory in that the measured pore water concentrations of NS and LS were considerably larger than the predicted values. This conclusion does not apply for gluconate, because its concentration in cement pore water was below the detection limit of approximately 50 nM.

Anion Exchange Resins↗
PubMed1998

Prospective comparison of intravenous quinidine and intravenous procainamide in patients undergoing electrophysiologic testing.

BACKGROUND: Intravenous procainamide hydrochloride is frequently used in the acute care setting and during electrophysiologic testing, but intravenous quinidine gluconate is rarely used because of concerns about its safety. This study prospectively compares the hemodynamic and electrophysiologic effects of these agents in patients undergoing electrophysiologic testing. METHODS AND RESULTS: Sixty-five consecutive patients with inducible ventricular tachyarrhythmias were prospectively treated with either intravenous quinidine gluconate or intravenous procainamide hydrochloride in an alternating unblinded fashion. The hemodynamic and electrophysiologic effects of these two drugs were compared. Seven (22%) patients assigned to intravenous quinidine gluconate and eight (24%) patients assigned to intravenous procainamide hydrochloride were rendered noninducible for ventricular tachyarrhythmias. Four (13%) patients assigned to intravenous quinidine gluconate were unable to complete the infusion compared with none (p = 0.05) assigned to intravenous procainamide hydrochloride. Otherwise, the overall hemodynamic and electrophysiologic effects of the two drugs were similar. CONCLUSIONS: Intravenous quinidine gluconate is a reasonable alternative to intravenous procainamide hydrochloride in patients requiring a parenteral type IA antiarrhythmic agent.

Aged↗