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Biomedical subjects

R H Briant

Publications and source records attributed to R H Briant.

16 recordsLinked to original sources
PubMed1978

Sodium valproate (Epilim) in epilepsy: a trial.

Of thirty-five patients with various types of epilepsy treated with sodium valproate, 15 achieved complete seizure control on that drug alone, 12 other patients benefited and eight failed to improve on the drug. Excellent results were more likely in those with petit mal epilepsy and in those whose epilepsy was controlled with other drugs at the expense of side effects. Three patients were unable to tolerate valproate, but in general few patients experienced side effects and several patients felt much better on valproate than on their previous drugs. A twice daily dosage regime was satisfactory. Plasma valproate levels at the final dose covered a wide range, 0.21 - 1.2mmol/l (34 to 190 microgram/ml) and did not correlate with response, lack of response or side effects.

Adolescent↗
PubMed1975

Metabolism of delta1-tetrahydrocannabinol by the isolated perfused dog lung. Comparison with in vitro liver metabolism.

The metabolism of (-)-delta1-tetrahydrocannabinol (delta1-THC) has been studied in the isolated perfused dog lung. After intravascular administration of [3H]-delta1-THC there was an overall biotransformation of 12%. Two major metabolites were isolated and identified as 3'-hydroxy-delta1-THC and 4'-hydroxy-delta1-THC. 7-Hydroxy-delta1-THC was also present together with small amounts of 6alpha-hydroxy-delta1-THC and 6beta-hydroxy-delta1-THC. An in vitro experiment using a dog liver microsomal preparation was also carried out and showed that the major metabolites were 6beta-hydroxy-delta1-THC and 6alpha-hydroxy-delta1-THC. 7-Hydroxy-delta1-THC and 1,2-epoxy-hexahydrocannabinol were also isolated together with small amounts of 3'-hydroxy-delta1-THC and 4'-hydroxy-delta1-THC. The side-chain hydroxylated compounds are hitherto undescribed metabolites of delta1-THC.

Animals↗
PubMed1975

Metabolism of nicotine by the isolated perfused dog lung.

1. Metabolism of [14C]nicotine has been studied in the isolated perfused dog lung. [14C]Nicotine, 50 mug every 30 s for 10 min administered via the pulmonary artery, undergoes first pass metabolism to a small extent. [14C]Cotinine was detected in the venous blood. Of the injected activity, 6 percent was in the lung at the end of experiment; 60 percent being present as [14C]nicotine and 20 percent as [14C]nicotine-1'-oxide. 2. When [14C]nicotine was administered in cigarette smoke a greater degree of metabolism was observed at first pass. Pyrolysis products of [14C]nicotine also were present in the venous blood. Lungs after smoke exposure contained 30 percent of administered radioactivity, with a substantial proportion of [14C]nicotine-1'-oxide. 3. Administration of [14C]nicotine-labelled smoke to lung preparations, on closed circuit, gave significant amounts of [14C]cotinine and other metabolites over a 2 h period. Lung tissue contained approx. 40 percent of injected dose, of which 25 percent only was [14C]nicotine. Large proportions of [14C]cotinine and [14C]nicotine-1'-oxide were present but 45 percent of the activity was present as other unidentified pyrolysis products. [14C]Demethyl cotinine was detected.

Animals↗
PubMed1974

Metabolism of isoprenaline after aerosol and direct intrabronchial administration in man and dog.

1 Administration of isoprenaline by aerosol inhalation to man results in over 80% being metabolized to the sulphate conjugate.2 The majority of an inhaled dose is probably swallowed since the metabolic pattern resembles that after an oral dose.3 Isoprenaline, administered in aqueous solution directly into the bronchial tree in both man and dog, is rapidly O-methylated to 3-O-methyl isoprenaline, which is subsequently conjugated with sulphate.4 3-O-Methylation is the main metabolic pathway for the small part of an inhaled dose which does enter the bronchial tree.

Administration, Topical↗
PubMed1973

Interaction between clonidine and desipramine in man.

Interaction between the tricyclic antidepressant desipramine and the antihypertensive agent clonidine has been investigated in five hypertensive patients in a double-blind placebo controlled study. Introduction of the tricyclic antidepressant led to loss of blood pressure control in four of the patients. The average blood pressure rise in the desipramine period compared with the placebo period was 22/15 mm Hg in the lying position and 12/11 mm Hg standing. Thus addition of a tricyclic antidepressant may lead to loss of blood pressure control in a hypertensive patient treated with clonidine.

Adult↗
PubMed1973

Assessment of selective beta-adrenoceptor blockade in man.

1. Selective antagonism of the cardiac beta(1)-adrenoceptors has been studied in normal human volunteers.2. Practolol and UK 6558 produced greater antagonism of the chronotropic and inotropic responses to i.v. isoprenaline than of the vasodilator response to either i.v. or intra-arterial isoprenaline. A third drug, M&B 17,803A, produced non-selective beta-adrenoceptor blockade in 2 of 3 subjects studied.3. Practolol, UK 6558 and M&B 17,803A, produced an attenuation of the responses to Valsalva's manoeuvre.4. A substantial reduction in blood pressure was seen in 3 of 4 normotensive subjects given UK 6558.

Adrenergic beta-Antagonists↗