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Biomedical subjects

P Hartvig

Publications and source records attributed to P Hartvig.

At least 235 records · Page 13Linked to original sources
PubMed1975

Electron-capture gas chromatography of methadone after oxidation to benzophenone.

A procedure for the determination of low levels of methadone (6-dimethylamino-4,4-diphenylheptanone-3) in serum has been developed. Methadone is extracted from serum into n-heptane and re-extracted into an acidic aqueous phase. Methadone is oxidized to benzopheone with barium peroxide in sulphuric acid, during which procedure an n-heptane phase is present into which the oxidation product is continuously extracted. The benzophenone formed is determined by means of electron-capture gas chromatography. The recoveries are 100 +/- 3% and 100 +/- 4.5% at the 120 and 16 ng levels, respectively. The minimum amount that can be determined in 1 ml of serum is 4 ng. Interferences from possible metabolies are probably minor. The main cyclic metabolite is only co-determined to a minor extent if the oxidation time is optimized. Comparison of this oxidation method with a combined gas chromatographic-mass spectrometric determination with selected ion monitoring showed identical serum levels.

Benzophenones↗
PubMedDate not supplied

Tacrine restores cholinergic nicotinic receptors and glucose metabolism in Alzheimer patients as visualized by positron emission tomography.

Three patients with Alzheimer's disease, a 68-year-old woman with mild dementia and 2 men (aged 64 and 72 years) with moderate dementia were treated orally with the cholinesterase inhibitor tacrine (tetrahydroaminoacridine), 80 mg daily, for several months. The patients were investigated using positron emission tomography (PET) prior to, and after 3 weeks and 3 months of treatment. The PET studies involved a multi-tracer system consisting of [18F]-fluoro-deoxy-glucose (18F-FDG) (tracer for glucose metabolism); 11C-butanol (cerebral blood flow) and (S)(-)- and (R)(+)-[N-11C-methyl]-nicotine (nicotinic receptors; cholinergic neural activity). Tacrine treatment increased the uptake of 11C-nicotine to the brain. Significant reduced difference in uptake between the two enantiomers (S)(-)- and (R)(+)11C-nicotine was observed in the frontal and temporal cortices after tacrine treatment in all three patients. The kinetic analysis indicated increased binding of (S)(-)11C-nicotine in brain compatible with a restoration of nicotinic cholinergic receptors. The most pronounced effect was observed after 3 weeks and 3 months treatment in the patient with mild dementia. An increase in cerebral glucose utilization was found in the 68-year-old patient with mild dementia but also slightly in the 64-year-old man with moderate dementia when treated with tacrine for 3 months. Tacrine administration did not affect cerebral blood flow. The PET data obtained after 3 weeks of tacrine treatment was paralleled by improvement in neuropsychological performance. This study shows in vivo by PET neurochemical effects induced in brain by treatment with tacrine to Alzheimer patients. Intervention with tacrine in the early course of the disease might be necessary for clinical improvement.

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