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Biomedical subjects

F Buneaux

Publications and source records attributed to F Buneaux.

At least 19 recordsLinked to original sources
PubMed1995

Pharmacokinetics of lithium in plasma and red blood cells in acute and chronic intoxicated patients.

Lithium disposition in plasma, red blood cells (RBC) and urine was studied in acute self-poisoned patients upon chronic lithium therapy (n = 4) and in chronic intoxicated patients receiving oral lithium (n = 10). Following acute intoxication upon chronic lithium therapy, lithium pharmacokinetics did not differ from previous reports. Terminal plasma half-life ranged from 19.0-29.0 h and RBC/plasma ratio was 0.32 +/- 0.11. The distribution volume of the terminal phase, Vz, was estimated at 0.84 +/- 0.32 l/kg and renal clearance was 0.38 +/- 0.11 ml/mn/kg. After chronic intoxication lithium pharmacokinetics differed from those of the acute patients. Terminal plasma half-life ranged from 36.5-79.4 h and zero-order decline appeared in 8 of the 10 patients. The RBC/plasma ratio was 0.87 +/- 0.22 on admission. Vz was estimated at 0.71 +/- 0.27 l/kg and renal clearance was 0.16 +/- 0.07 ml/mn/kg. These modifications in lithium elimination kinetics could be related to the decrease in the glomerular filtration rate with age or renal dysfunction in this group of patients.

Administration, Oral↗
PubMed1994

Study of the mechanisms involved in hydroxocobalamin interference with determination of some biochemical parameters.

Hydroxocobalamin (OHCo), a red pigment used as an antidote in cyanide poisoning, interferes with determination of some biochemical parameters. Plasma pools were spiked with two concentrations of OHCo and eight parameters (CK, SGOT, SGPT, ALP, lactic acid, creatinine, glucose, bilirubin) were assayed using Dimension and Aca III automated analyzers (Du Pont Instruments). Two parameters were affected by the presence of OHCo: CK and bilirubin. This study documents the type of interferences, spectral or chemical, and its probable causes.

Artifacts↗
PubMed1989

[Assay of total mercury in blood, plasma and erythrocytes by emission spectrometry-induced plasma HF (SEPIHF)].

The mercury quantification in blood can be performed by ICPAES after dilution in an ammonia buffer and reduction by sodium borohydride. The proposed method does not need mineralization. The sample is not nebulized in the torch but the mercury vapor, after collection in a reactor vial, is swept into the plasma by the carrier gas (argon) using the described glass apparatus, and quantified at lambda = 253.65 nm.

Erythrocytes↗
PubMed1981

[Treatment of rheumatoid arthritis with zinc sulfate. Results of a doubl-blind trial].

At the end of a double blind clinical test carried out in 35 patients with classical rheumatoid arthritis, or progressive and with certain diagnosis, it does not appear that zinc sulphate given by mouth at dose of 600 mg/24 hours (divided up into 3 doses) may be a valid basic treatment. In fact, none of the classical clinical criteria (Richtie index, Lee index, etc.) nor laboratory criteria (E.S.R.) show any statistically significant change after 4 and 8 months. The discrepancy between these results and those previously published in discussed.

Arthritis, Rheumatoid↗
PubMed1978

[Zinc and enzymes in the synovial fluid and blood in various types of rheumatism].

It appears that in rheumatoid arthritis and, to a lesser extent, in the other forms of inflammatory rheumatism, the level of zinc in the blood serum is lowered, whereas synovial zinc is increased. In the synovial fluid, there is a very significant correlation between enzyme activity and the concentration of zinc. Practical experiments aimed at demonstrating in vitro the action of zinc on lacticodeshydrogenase, acid phosphatase, lysozyme and beta-glucuronidase did not produce the anticipated results and do not explain the metabolic disorders of zinc seen during inflammatory rheumatisms.

Acid Phosphatase↗
PubMed1977

[Automated measurement of elastase activity and elastase inhibitory capacity of serum].

A technic of autoanalysis of the elastase activity and the capacity of elastase inhibition of the serum is described. This estimation depends on the hydrolysis by elastase of N-ter-butoxycarbonyl-L-nitrophenyl ester with liberates p.nitrophenol the colour of which is read at 405 nm. The means of this sample estimation are reported in a few cases of respiratory, dermatological and pancreatic disease.

Animals↗
PubMed1977

[The effect of osmic acid on synovial and serum beta-glucuronidase activity].

The authors report that osmic acid, in vitro, increases the activity of beta-glucuronidase in serum and synovial, ascitic and pleural fluids, whereas five other metals of similar molecular weight (platinum, gold, mercury, thallium and lead) are either inactive or inhibitory. By contrast the osmium diminishes the activity of LDH and acid phosphatases in serum and synovial fluid. This effect on beta-glucuronidase is thought to be due to inhibition of a natural inhibitor present in biological fluids, a protein found by several authors.

Acid Phosphatase↗
PubMed1975

[Several synovial enzymes in rheumatoid arthritis].

The authors show that although the enzyme variations are nil or unimportant in the mechanical joint fluids, they are of some importance in the inflammation fluids, particularly in cases of rheumatoid arthritis. Of those studied so far, the variations are most notable in the dehydrogenases and the phosphatases, the variations being highly significant and related to one another and to the sedimentation rate.

Acid Phosphatase↗
PubMed1973

[Chrysotherapy].

Explore the source record for details and available documents.

Animals↗
PubMedDate not supplied

Continuous flow quantification of total mercury in whole blood, plasma, erythrocytes, and urine by inductively coupled plasma atomic emission spectroscopy.

Mercury determination in blood and urine can be performed by inductively coupled plasma atomic emission spectroscopy (ICPAES) after dilution in an ammonia buffer and reduction by sodium borohydride. The proposed method does not need an oxidative mineralization. The sample is not nebulized into the torch, but the mercury vapor, after collection in a reactor vial, is swept into the plasma by the argon carrier gas using the described glass apparatus.

Erythrocytes↗
PubMedDate not supplied

Determination of hydroxocobalamin and cyanocobalamin by derivative spectrophotometry in cyanide poisoning.

Hydroxocobalamin (OHCo) and cyanocobalamin (CNCo) are determined directly in biological media, without extraction, by using first derivative spectrophotometry. We diluted 200 mL of plasma, urine, or standards with 1.8 mL of pH 6 buffer (boric acid, potassium dihydrogen orthophosphate, and potassium hydroxide). The first derivative spectra of the dilutions were plotted between 320 and 400 nm. At the exact zero-crossing point for hydroxocobalamin, the derivative values of cyanocobalamin concentration were determined. The same procedure was followed for hydroxocobalamin at the zero-crossing point for cyanocobalamin. The derivative values of the concentration curves are linear in the range 5-100 microM. The minimum detection limit is approximately 5 microM for hydroxocobalamin of cyanocobalamin on the determination of hydroxocobalamin or vice versa, although the spectra strongly overlap. The method is fast and simple to use, thus making it easy to assess the in vivo transformation of hydroxocobalamin into cyanocobalamin after the administration of high doses of hydrocobalamin in cyanide poisoning.

Cyanides↗