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Biomedical subjects

D F Sharman

Publications and source records attributed to D F Sharman.

At least 73 records · Page 4Linked to original sources
PubMed1975

The estimation of 3,4-dihydroxyphenylacetic acid, homovanillic acid and homo-isovanillic acid in nervous tissue by gas-liquid chromatography and electron capture detection.

1 A gas chromatographic method using electron capture detection is described for the estimation of three acidic metabolites of dopamine, 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid, HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-hydroxy-4-methoxyphenylacetic acid (homo-isovanillic acid, iso-HVA). The method is based on the formation of the trifluoroacetyl-hexafluoroisopropyl derivatives of the three acids. 2 The method has been applied to the estimation of DOPAC, HVA and iso-HVA in tissues from the central and peripheral nervous systems.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1975

Postnatal development of dopamine deamination in the striatum of the rat.

In the striata of litter-mate rats the development of the monoamine oxidase (MAO) activity towards dopamine in vitro followed a similar time course with age as the tissue concentrations of homovanillic acid and dihydroxphenylacetic acid, the two acid metabolites of dopamine formed by the action of MAO.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1974

The effect of tranquillizing drugs on the concentration of the sulphate ester of 4-hydroxy-3-methoxyphenylethane-1,2-diol in rat brain.

A total of 17 butyrophenone, phenothiazine, benzodiazepine and imidazoline tranquillizing drugs were examined for their ability to increase the cerebral concentration of the sulphate ester of 1(4-hydroxy-3-methoxyphenyl)ethane-1,2-diol (MHPG-SO(3) H), a metabolite of noradrenaline in the rat brain. Of these drugs, when given in a dose of 10 mg/kg i.p., only trifluperidol, haloanisone, azaperone, clozapine and haloperidol were found to increase the cerebral concentration of MHPG-SO(3) H. This effect is unrelated to the ability of such drugs to antagonize the lethal effects of an intravenous injection of noradrenaline and suggests that the properties of the central noradrenaline receptors differ from those of the peripheral noradrenaline receptors.

Animals↗
PubMed1974

Studies on the metabolism of catecholamines in the central nervous system of the mouse.

1 The distribution of the metabolites of noradrenaline, 1-(3,4-dihydroxyphenyl)ethane-1,2-diol (DOPEG) and 1-(4-hydroxy-3-methoxyphenyl)ethane-1,2-diol (MOPEG), in the brain of the mouse has been investigated.2 The rate of disappearance of the metabolites after inhibition of the enzyme monoamine oxidase has been used to estimate their turnover rates in the mouse hypothalamus. It was concluded that the turnover of DOPEG was much faster than that of MOPEG.3 When mice were treated with reserpine dissolved in 5% ascorbic acid solution there was an increase in the hypothalamic concentration of both MOPEG and DOPEG. However, similar increases in the concentrations of the two metabolites were seen when the animals were treated with 5% ascorbic acid solution alone.4 The administration of tropolone, an inhibitor of the enzyme catechol-O-methyl transferase, resulted in an increase in the concentration of DOPEG.5 Mice, exposed to a temperature of -15 degrees C showed increased hypothalamic concentrations of both DOPEG and MOPEG.6 The rates of formation in the mouse striatum of 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxyphenylacetic acid (HVA), acidic metabolites of dopamine, were compared with the turnover rate of dopamine, estimated from the rate at which this catecholamine disappears after treatment with alpha-methyl-p-tyrosine. It was concluded that the estimate of dopamine turnover obtained by this method is likely to be too large because of the compensatory feedback mechanism which is thought to play a role in the metabolism of dopamine in the brain.

Acetylation↗
PubMed1972

The effect of sodium -hydroxybutyrate on the metabolism of dopamine in the brain.

1. Sodium gamma hydroxybutyrate (GHB-Na), when given to rats and mice, caused a sleep-like state and a fall in body temperature of about 10 degrees C.2. GHB-Na produced a dose-dependent increase in the concentration of dopamine (DA) in the brains of mice kept at an environmental temperature of 18-20 degrees C or 30-32 degrees C.3. The concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxyphenylacetic acid (HVA), the metabolites of DA, were increased in the striatal tissues of rats and mice, after the administration of GHB-Na. However there was a delay of 60 min before the concentration of HVA increased whereas there appeared to be little delay before the concentration of DOPAC increased.4. When GHB-Na was administered to reserpine-treated animals, no increase occurred in the concentration of dopamine in the brains of mice or rats, or of DOPAC in the rat brain.5. Reserpine did not prevent the induction of the sleep-like state by GHB-Na.6. The results presented suggest that the effect of GHB-Na in increasing the concentration of DA requires unimpaired storage mechanisms for the amine.

Animals↗