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Biomedical subjects

D B Calne

Publications and source records attributed to D B Calne.

At least 307 records · Page 17Linked to original sources
PubMed1970

Miosis during L-dopa therapy.

The pupillary diameter of 11 patients with Parkinson's disease was significantly decreased four hours after ingestion of L-dopa. It is suggested that this miosis may be caused by diminished noradrenaline output at sympathetic nerve endings, or alternatively by an action on the central nervous system.

Aged↗
PubMed1970

Hypotension caused by L-dopa.

In 20 patients with idiopathic Parkinsonism maximum tolerated doses of L-dopa were found to induce a mean reduction in blood pressure (erect systolic) of 19.3 mm.Hg, without any significant change in pulse rate. This hypotension may be due to dopamine, acting on adrenergic nerve endings or on the central nervous system itself.

Central Nervous System↗
PubMed1969

m-Hydroxyphenylacetic acid formation from L-dopa in man: suppression by neomycin.

The increased excretion of m-hydroxyphenylacetic acid in the urine of patients with parkinsonism being treated with L-dopa was reduced by gut sterilization with neomycin. The p-de-hydroxylation step is thus brought about solely by the action of gut flora; the pathway is unlikely to be involved in the events within the brain leading to the therapeutic benefit effected by L-dopa.

Dihydroxyphenylalanine↗
PubMed1969

Action of dopamine on the human iris.

Dopamine eye drops produce marked dilatation of the pupil in man. This mydriatic effect is inhibited by pretreatment with guanethidine. It is therefore concluded that dopamine acts indirectly via adrenergic nerve endings, rather than exerting a direct effect on adrenergic receptors in the dilator pupillae muscle. In this respect dopamine resembles the phenyl-alkylamines, such as tyramine, rather than the catecholamines, adrenaline and noradrenaline.If dopamine acts by releasing noradrenaline from adrenergic nerve endings, high concentrations of dopamine could lead to depletion of noradrenaline stores, since synthesis might be unable to keep pace with release. This could be the explantion for the orthostatic hypotension found in patients taking L-dopa for Parkinsonism.

Adult↗
PubMed1969

The metabolism of orally administered L-Dopa in Parkinsonism.

1. Gas-liquid chromatographic methods were used to measure urinary acidic and alcoholic metabolites of L-DOPA, which had been administered in high oral dosage to patients with postencephalitic and idiopathic Parkinsonism.2. The output of these compounds was normal before treatment. During drug therapy, large quantities of the dopamine metabolites, homovanillic acid and dihydroxyphenylacetic acid, were excreted but traces only of 4-hydroxy-3-methoxyphenylethanol. Noradrenaline metabolites showed little change in output other than a small increase in 4-hydroxy-3-methoxymandelic acid.3. Information was obtained about a number of minor routes of degradation which might be implicated in the therapeutic action of L-DOPA. A raised output of m-hydroxyphenylacetic acid pointed to p-dehydroxylation of dihydroxyphenylacetic acid by gut flora. Evidence of transamination as a minor metabolic pathway was obtained by finding appreciable urinary levels of 4-hydroxy-3-methoxyphenyllactic acid. A keto-acid precursor of this compound may act as competitive inhibitor of an enzyme active in the normal degradation route of tyrosine, p-hydroxyphenylpyruvic acid oxidase, for increased amounts of p-hydroxyphenyllactic acid, the major metabolic derivative of p-hydroxyphenylpyruvic acid, accumulated in the urine during DOPA treatment.

Chromatography, Gas↗
PubMed1969

Tremor induced by tetrabenazine.

1. Acute administration of tetrabenazine produced tremor in cats, in doses which caused sedation but not hypothermia.2. The pattern of movements resembled shivering rather than Parkinsonism, and warming the skin suppressed the tremor.3. The tremor was not influenced by hyoscine.4. Tremor produced by amylobarbitone was essentially similar to that induced by tetrabenazine.

Amobarbital↗