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Biomedical subjects

J A Vale

Publications and source records attributed to J A Vale.

At least 109 records · Page 6Linked to original sources
PubMed1986

Treatment of phenobarbitone poisoning with repeated oral administration of activated charcoal.

Six patients with moderate to severe phenobarbitone intoxication were treated with repeated oral doses (50 g) of activated charcoal following an initial dose of 50 to 100 g. All recovered more rapidly than would otherwise be expected with supportive care alone. The mean maximum rate of fall in plasma phenobarbitone concentrations corresponded to a half-life of only 6.2 +/- 2.5 h (normally three to five days); 62 to 93 per cent of the absorbed dose was eliminated within 24 h and the mean total body clearance of the drug during and for up to 12 h after administration of charcoal was 84 +/- 34 ml/min. Treatment with repeated oral doses of activated charcoal is simple and safe. It seems to be as effective as forced alkaline diuresis, haemodialysis and haemoperfusion for the removal of phenobarbitone following overdosage.

Administration, Oral↗
PubMed1984

Epidemiology of analgesic overdose in England and Wales.

The number of deaths from acute poisoning in England and Wales has remained constant at approximately 4000 per annum for the last 10 years despite major changes in the agents responsible. Deaths due to carbon monoxide and barbiturate and non-barbiturate hypnotics have fallen, while those due to psychotropic and analgesic drugs have risen. The number of hospital admissions in England and Wales due to analgesics taken in overdose has risen from 15 940 in 1968 to 24 930 in 1980, with aspirin and paracetamol being the preparations most commonly ingested. Currently, the mortality from salicylate intoxication is falling while that due to paracetamol is rising. In 1980, the Office of Population Censuses and Surveys recorded 790 deaths from analgesic poisoning, of which 181 were due to salicylates and 152 to paracetamol alone. A further 269 deaths were attributed to paracetamol and dextropropoxyphene, and an additional 132 deaths were thought to be due to paracetamol in combination with other drugs. An important factor in the changing mortality from salicylate and paracetamol poisoning is the trend observed in the sales and usage of these agents. Since 1979, the number of analgesic tablets containing aspirin sold in the UK (except Northern Ireland), excluding hospital use, has fallen by 326 X 10(6), while sales of those containing paracetamol have increased by 395 X 10(6) tablets.

Acetaminophen↗
PubMed1984

Dextropropoxyphene poisoning: problems with interpretation of analytical data.

Difficulties in the estimation and interpretation of dextropropoxyphene and norpropoxyphene analyses have added to the controversy concerning the toxicity of these compounds. Poor performance in external proficiency assessment trials reflects the unsatisfactory state of many dextropropoxyphene and norpropoxyphene analyses in general use. There is substantial overlap between blood concentrations of dextropropoxyphene and norpropoxyphene encountered in chronic therapeutic dose and those associated with acute toxicity. As dextropropoxyphene and norpropoxyphene are often taken in overdose with other drugs, their blood concentrations must be interpreted in the context of careful identification and quantitation of such agents. The present availability of accurate methods for measurement of parent drug and metabolite should now make anecdotal reports unsupported by analytical data entirely superfluous.

Dextropropoxyphene↗
PubMed1984

Deaths from paracetamol and dextropropoxyphene (Distalgesic) poisoning in England and Wales in 1979.

Paracetamol and dextropropoxyphene were implicated on clinical and analytical grounds in 237 poison deaths in England and Wales in 1979. In addition to paracetamol, dextropropoxyphene and ethanol, other agents were detected in 61 of these cases (26%). Analytical evidence suggests that very substantial overdoses of paracetamol and dextropropoxyphene were ingested in the majority of cases; their mean plasma concentrations in those ingesting no other agents were 252 and 8.64 mg/l respectively. Significant quantities of ethanol were ingested in 133 of 237 cases (56%). The mean ethanol concentration in those in whom quantitative estimations of paracetamol, dextropropoxyphene and ethanol were undertaken and who had not ingested other drugs, was 1588 mg/l. There was no analytical support for the diagnosis of paracetamol and dextropropoxyphene poisoning in 74 of 305 cases (24%) of H.M. Coroners' returns to the Office of Population, Censuses and Surveys for the period 1 January-31 December 1979. In addition, dextropropoxyphene was detected analytically in six cases classified as being due to paracetamol alone.

Acetaminophen↗
PubMed1983

The effects of oestrogen administration on tryptophan metabolism in rats and in menopausal women receiving hormone replacement therapy.

The effects of the administration of oestrogens on the activity of hepatic tryptophan oxygenase have been assessed both directly (by measurement of enzyme activity in vitro) and indirectly (by measurement of urinary excretion of tryptophan metabolites) in rats, and indirectly in menopausal women receiving hormone replacement therapy. Intraperitoneal administration of 500 micrograms of oestradiol or ethinyl oestradiol/kg body wt had no effect on the activity of tryptophan oxygenase in homogenates of liver from mature (13-week-old) female rats. Both adrenalectomy and ovariectomy led to a reduction in the activity of tryptophan oxygenase in homogenates of liver from mature rats; again there was no effect of giving 500 micrograms of oestradiol/kg body wt by intraperitoneal injection. Intraperitoneal administration of 210 micrograms of oestrone sulphate/kg body wt for 1 or 2 days before killing, or its incorporation in the diet for up to 8 weeks at an equivalent dose rate, had no effect on the activity of tryptophan oxygenase in homogenates of liver from ovariectomized 6-14-week-old female rats. Intraperitoneal administration of 500 micrograms oestradiol/kg body wt to intact mature female rats together with 500 mg tryptophan/kg body wt caused a reduction in the urinary excretion of xanthurenic and kynurenic acids, kynurenine and N1-methyl nicotinamide. When peri- and post-menopausal women were treated with ethinyl oestradiol (20 micrograms/day) or piperazine oestrone sulphate (3 mg/day) for 3 months, there was an increase in the concn of tryptophan in plasma, with no change in the urinary excretion of xanthurenic and kynurenic acids and kynurenine. This study provides no evidence for the induction of tryptophan oxygenase by oestrogens in rats or human beings.

Adrenalectomy↗
PubMed1983

High-performance liquid chromatographic measurement of atenolol: methodology and clinical applications.

A simple high-performance liquid chromatographic method has been developed for the measurement of atenolol in plasma, breast milk, and urine. The sample (250 microliters) is Vortex-mixed for 30 s with approximately 50 mg sodium chloride, 10 mol/L sodium hydroxide solution (50 microliters), internal standard solution (aqueous benzimidazole, 1.69 mumol/L) (50 microliters) and methyl-tert-butyl ether containing 10% (vol/vol) heptafluorobutanol (200 microliters). After centrifugation (9950 X g, 2 min), a portion (100 microliters) of the resulting extract is analysed on a microparticulate (5 micron) silica column using methanol containing 1 mmol/L d-10-camphorsulphonic acid monohydrate as the mobile phase, and the column effluent is monitored by fluorescence detection using an excitation wavelength of 195 nm. A specimen, together with a quality control sample, can be analysed in duplicate within 30 min. The limit of accurate measurement of the assay is 20 micrograms/L, no endogenous sources of interference have been observed and interference from other drugs is minimal.

Adult↗