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Biomedical subjects

D B Barnett

Publications and source records attributed to D B Barnett.

At least 91 records · Page 5Linked to original sources
PubMed1983

Central and peripheral nerve conduction in thyroid dysfunction: the influence of L-thyroxine therapy compared with warming upon the conduction abnormalities of primary hypothyroidism.

1. The latencies of the visual evoked responses, indices of central nerve conduction, and peripheral nerve conduction were slowed in patients with primary hypothyroidism compared with controls. 2. In thyrotoxic patients, there was no change in the latencies of the visual evoked responses and peripheral nerve conduction compared with the control group. 3. The abnormalities seen in hypothyroidism were reversed by L-thyroxine therapy. 4. Warming untreated hypothyroid patients significantly improved both central and peripheral nerve conduction. 5. The conduction delay found in hypothyroidism is to a large extent dependent upon a subnormal body temperature.

Evoked Potentials, Visual↗
PubMed1983

The effects of diazepam and oxprenolol on short term memory in individuals of high and low state anxiety.

1 The effect of oral doses of diazepam (5 mg) and oxprenolol (80 mg) on short term memory of normal individuals stratified for 'state' anxiety levels has been investigated. 2 Normal student volunteers were stratified into high and low anxiety groups on the basis of responses to the Spielberger 'A-state' scale. Subjects were then randomly administered active drug or placebo and given a form of running memory test performed under a variety of conditions in which variable rate of item presentation and articulatory suppression were used. 3 Diazepam significantly reduced the errors of recall in the running memory test in the high anxiety group and produced a distinct separation of response from the low anxiety group under the test conditions of slow item presentation with articulatory suppression. Oxprenolol had no effect on the short term memory test in either high or low anxiety groups in any experimental test situation. 4 These results are compared to previous work in which generally a deleterious effect of diazepam on short term memory in normal volunteers has been reported. The implications of these findings are further discussed in relationship to possible models of memory function.

Adolescent↗
PubMed1982

[3H]Rauwolscine and [3H]yohimbine binding to rat cerebral and human platelet membranes: possible heterogeneity of alpha 2-adrenoceptors.

The specific binding of the alpha 2-adrenoceptor antagonists [3H]yohimbine and [3H]rauwolscine to membranes prepared from rat cerebral cortex and human platelets was rapid, reversible, saturable and of high affinity. Both ligands labelled an identical population of sites in cerebral or platelet membranes though the affinities of both agents were significantly lower in brain. The specific binding of [3H]yohimbine and [3H]rauwolscine in both tissues was displaced by various adrenergic agents in a manner that suggests that the labelled sites probably represent the alpha 2-adrenoceptor. There were, however, significant differences in the affinities of certain alpha-antagonists between cerebral and platelet preparations, even though these agents generated displacement curves with slopes close to unity in both tissues. Thus, whereas yohimbine, rauwolscine, WB4101 and corynanthine were all weaker in cerebral cortex, prazosin was significantly more potent at cortical than in platelet membranes. A possible heterogeneity of alpha 2-adrenoceptors is discussed.

Animals↗
PubMed1982

Disopyramide and its N-monodesalkyl metabolite in breast milk.

The plasma and breast milk were sampled from a woman who was breastfeeding whilst taking disopyramide (200 mg three times daily). Paired samples taken on the fifth to eighth day of treatment showed that disopyramide was present in breast milk in a similar concentration to plasma (mean +/- s.d. milk; plasma ratio 0.9 +/- 0.17). The estimated dose likely to be ingested by an infant is less than 2 mg kg-1 day-1. The active N-monodesalkyl metabolite of disopyramide (NMD) although present in plasma in much smaller concentrations than the parent compound, was excreted in breast milk (mean +/- s.d. milk: plasma ratio 5.6 +/2.9) in concentrations similar to those of disopyramide. The pharmacological and toxicological properties of the disopyramide metabolite need to be considered when assessing likely effects on the infant. No adverse effects were noted in the infant in this case. Maternal plasma and breast milk were sampled again along with infant plasma after 28 days. Disopyramide and NMD were undetectable in the infant's serum. No evidence was found to indicate that the concentrations of disopyramide or NMD in breast milk might be sufficient to pose a definite risk to the infant. Whenever disopyramide is prescribed in a breast feeding mother, close observation of the baby and measurement of both disopyramide and its active metabolite NMD in breast milk or infant plasma is recommended, pending further investigation.

Adult↗
PubMed1980

Evaluation of a radioreceptor assay for beta-adrenoceptor antagonists in plasma.

A radioreceptor assay (RRA) recently developed in this laboratory for beta-adrenoceptor antagonists in plasma was evaluated in normal volunteers and compared with a radioimmunoassay (RIA) for propranolol. The RRA depends upon the ability of beta-adrenoceptor antagonists to complete with a radiolabelled ligand for beta-adrenoceptor binding sites on lung membranes. Unlike other assays, it measures biologically active drugs including active metabolites of the parent compound. In volunteers given a single oral dose of (+/-)-propranolol, considerable differences between the two assay methods were demonstrated. In other experiments this difference was shown to relate to the RIA's sensitivity to the inactive (+)-isomer of propranolol and possibly to inactive metabolites. The facility of the RRA in measuring plasma levels of several other non-selective beta-adrenoceptor antagonists was also demonstrated. By employing (-)-propranolol as the standard in the RRA, all of these drugs can be directly compared with a single and relatively simple assay technique.

Adrenergic beta-Agonists↗
PubMed1979

Pharmacological characteristics of beta-adrenoceptor binding sites in intact and sympathectomized rat spleen.

[3H]-(--)-Dihydroalprenolol ([3H]-DHA) binds to rat spleen membranes with a dissociation equilibrium constant (KD) of about 0.7 nM and a maximal number of binding sites of 272 fmoles x mg protein-1. Approximately 90% of the sites labelled by 1 nM [3H]-DHA possess classical properties of beta-adrenoceptors. The labelled ligand is stereospecifically displaced by the isomers of propranolol and the order of potency of agonists is: isoprenaline greater than adrenaline greater than noradrenaline. Highly selective beta 1 antagonists such as practolol and atenolol displaced [3H]-DHA from spleen membranes in a biphasic manner indicating the co-existence of beta 1 and beta 2 sites (30--35% beta 1; 65--70% beta 2) in this tissue. Support for this classification was provided by the binding of the beta 2 agonist procaterol to spleen membranes. This drug possessed high affinity only for those sites that have low affinity for the beta 1 selective agents. Chemical sympathectomy induced by chronic 6-hydroxydopamine administration did not alter the number or the pharmacological properties of beta-adrenoceptor binding sites. The results suggest that both beta 1 and beta 2 adrenoceptors are probably postsynaptic in spleen.

Alprenolol↗
PubMed1978

Measurement of beta-adrenoceptor antagonists in biological fluids using a radioreceptor assay.

A new assay for plasma levels of beta-adrenoceptor antagonists is described. The assay depends upon the ability of the drug to compete with a labelled beta-adrenoceptor antagonist (-)-[3H]dihydroalprenolol for beta-adrenoceptor binding sites on lung membranes. The assay is simple to perform, very sensitive and does not require prior extraction of plasma. The assay can also detect bioactive metabolites of these agents and is clearly not limited to a single beta-adrenoceptor antagonist.

Adrenergic beta-Antagonists↗