Lack of effect of single high doses of buprenorphine on arterial blood gases in the rat.

High dose buprenorphine, a potent semisynthetic agonist-antagonist for opiate receptors, is now used in substitution treatment of human heroin addiction. Deaths have been reported in addicts misusing buprenorphine. We determined the median lethal dose (LD(50)) and studied the effects of high doses of intravenous buprenorphine on arterial blood gases in rats. Male Sprague-Dawley rats were administered buprenorphine intravenously to determine the LD(50) using the up-and-down method. Subsequently, catheterized groups of 10 restrained rats received no drug, saline, acid-alcohol aqueous solvent (required to dissolve buprenorphine at a high concentration), or 3, 30, or 90 mg/kg of buprenorphine intravenously. Serial arterial blood gases were obtained over 3 h. The LD(50) determined in triplicate was 146.5 mg/kg (median of 3 series, range: 142.6-176.5). The mean dose received by surviving animals was 96.9 +/- 46.7 mg/kg. There was a significant effect of the acid-alcohol aqueous solvent on arterial blood gases. Excluding the solvent effect, 3, 30, and 90-mg/kg buprenorphine doses had no significant effects on arterial blood gases. The toxicity of intravenous buprenorphine in adult rats, assessed by the LD(50), is low. These data are consistent with a wide margin of safety of buprenorphine. The mechanism of death after the intravenous administration of a lethal dose of buprenorphine remains to be determined.

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.

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.

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.

A rapid spectrophotometric blood cyanide determination applicable to emergency toxicology.

Cyanide determination in whole blood can be performed by spectrophotometry after using diffusion coupled with coloration by hydroxocobalamin in a Conway dish. The technique may be accelerated by the use of a heating sheet at 45 degrees C. The method proved to be specific, sensitive, and fast, thus permitting measurements in emergency situations.

[Assay of total mercury in blood, plasma and erythrocytes by emission spectrometry-induced plasma HF (SEPIHF)]. / Dosage du mercure total dans le sang, le plasma et les érythrocytes par spectrométrie d'émission--plasma induit 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.

[Automated measurement of elastase activity and elastase inhibitory capacity of serum]. / Dosage automatique de l'activité élastasique et de la capacité d'inhibition élastasique du sérum.

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.

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.

[Risk of underestimating blood carbon monoxide by certain analytic methods]. / Risque de sous-estimation de l'oxycarbonémie lié à certaines méthodes de mesure.

OBJECTIVE: Study the effect of delay to assay on the measurement of carboxyhemoglobin (HbCO) in total blood samples. METHODS: Carbon monoxide (CO) and carboxyhemoglobin were measured on 75 blood samples drawn from healthy subjects (smokers and non smokers) and in subjects with carbon monoxide (CO) poisoning. Blood samples were drawn on lithium heparinate in perfectly closed tubes with no head space and stored at 4 infinity C until assay. The samples were pooled into 4 classes for 4 delays to assay: immediate, less than one hour, 3 hours, 12 hours. Infrared spectrometry was used to assay CO and order 4 and 5 derived spectrophotometry using CO-oximeters (AVL 912, IL 482, Corning 270, Radiometer OSM 3, Radiometer ABL 520) for HbCO. RESULTS: Regression lines for CO versus HbCO suggested that oxycarbonemia was underestimated using techniques measuring HbCO. This underestimation varied from 3 to 40% for delays to assay of 0 to 3 hours. CONCLUSION: Clinicians should be aware that the underestimation in oxycarbonemia related to HbCO assays is sensitive to delay to assay.

[Several synovial enzymes in rheumatoid arthritis]. / Quelques enzymes synoviales dans la polyarthrite rhumatoïde

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.

[Zinc and enzymes in the synovial fluid and blood in various types of rheumatism]. / Zinc et enzymes dans le liquide synovial et le sang au cours de rhumatismes divers.

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.

[The effect of osmic acid on synovial and serum beta-glucuronidase activity]. / Action de l'acide osmique sur l'activité de la bêta-glucuronidase synoviale et sérique.

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.

[Role of the laboratory in the diagnosis and treatment of lead poisoning]. / Rôle du laboratoire dans le diagnostic et le traitement d'une intoxication par le plomb

A case of therapeutic lead poisoning in a six-week old child is reported, this aetiology being very common in paediatrics. The role of the laboratory in treatment is described, the latter having involved the addition of disodium calcitetracemate to the peritoneal dialysis fluid.

[Treatment of rheumatoid arthritis with zinc sulfate. Results of a doubl-blind trial]. / Traitement de la polyarthrite rhumatoïde par le sulfate de zinc. Résultat d'un essai en double aveugle.

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.

Ferrocyanide ingestion may cause false positives in cyanide determination.

CASE REPORT: The authors present a patient who ingested a cyanide containing solution and arrived at the hospital without any clinical evidence of intoxication but an elevated blood cyanide level. The authors explain this discrepancy with the following hypotheses: 1) the patient ingested cyanide as an iron-chelated complex; and 2) the sulfuric acid used in the standard microdiffusion technique released cyanide from its iron-bound state to result in the observed elevated blood cyanide. Through a series of in vitro analyses, the authors demonstrate the following: 1) the ingested solution tested positive for cyanide with the sulfuric acid technique and negative for cyanide with acetic acid; 2) the presence of a ferrous salt in the ingested product by a colorimetric redox titration technique; and 3) release of a small fraction of the total cyanide from ferrocyanide by the sulfuric acid technique. The authors conclude: 1) the patient ingested potassium ferrocyanide; and 2) the strong acid used in the cyanide microdiffusion assay will liberate cyanide that is chelated to iron to yield false positive results.