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Biomedical subjects

H Hall

Publications and source records attributed to H Hall.

At least 181 records · Page 10Linked to original sources
PubMed1984

Acute effects of atypical antidepressants on various receptors in the rat brain.

Using in vitro receptor binding techniques, the effects of a number of different antidepressants on rat cerebral cortex receptors were investigated. In contrast to the tricyclic antidepressants, which potently inhibit several postsynaptic receptors, many atypical antidepressants have no or very little affinity for these receptors. Thus bupropion, amineptine, citalopram, fluoxetine, fluvoxamine and viloxazine are devoid of any activity, while amoxapine, doxepin and trazodone exert effects on a number of receptors. The implications of these receptor blocking effects are discussed.

Animals↗
PubMed1984

Characterization of the binding of 3H-norzimeldine, a 5-HT uptake inhibitor, to rat brain homogenates.

The binding of radiolabelled norzimeldine, a potent selective 5-HT reuptake inhibitor, to rat brain homogenates is described. 3H-Norzimeldine binds to a site with high affinity (KD = 10.5 nM) in a saturable manner (Bmax = 15.4 pmol/g wet weight in the cerebral cortex). The number of binding sites in the various regions of the brain parallels the capacity of the 5-HT reuptake mechanism. Drugs that inhibit the reuptake of 5-HT are also potent inhibitors of the 3H-norzimeldine binding, as are the tricyclic antidepressants, which are non-specific inhibitors of the noradrenaline and the 5-HT reuptake. Lesioning experiments using DSP4 (a NA neurotoxin) and p-chloroamphetamine (a 5-HT neurotoxin) suggest that the binding site is located on the presynaptic 5-HT nerve terminal, although a small component of the binding may be to noradrenergic uptake sites as well.

Animals↗
PubMed1984

Effect of lipophilicity of substituted benzamides on the dopaminergic effects in vivo and in vitro.

The antidopaminergic potencies of some new substituted benzamides related to remoxipride have been studied in the rat using in vitro (3H-spiperone binding) and in vivo techniques (antagonism of apomorphine induced stereotypies). The lipophilicities of the different benzamides were calculated by the addition of the lipophilic contribution (pi value) of the added substituent. It was found that the in vivo potencies of the compounds were not direct proportional to the in vitro potencies. The discrepancies in the potencies in vitro and in vivo (expressed as the ratio) are correlated to the calculated lipophilicities. Certain substituents in the benzene nucleus affect this in vitro--in vivo ratio more than could be expected from the change in lipophilicity caused by the substituent. The type of side chain is also of great importance. The reasons for the discrepancies between in vitro and in vivo antidopaminergic potencies of the studied substituted benzamides are discussed.

Animals↗
PubMed1984

Hypersensitivity to dietary components in young farm animals: isolation and partial purification of bovine immunoglobulin E.

An antibody of known specificity and active in long (72 hours) latent period passive cutaneous anaphylactic reactions, was isolated and partially purified from bovine serum. This antibody was not associated with immunoglobulins IgG, IgM or IgA. A rabbit antiserum raised against this antibody and used as an immunoabsorbent, successfully recovered skin sensitising antibody from bovine reaginic serum.

Animals↗
PubMed1984

Haloperidol inhibition of monoamine oxidase in vivo and in vitro.

Haloperidol was found to inhibit monoamine oxidase (MAO) activity in sonicated platelets by 50% (IC50) at a concentration of 10(-4) M. Preincubation of the sonicated platelets with haloperidol before the assay did not shift the dose-response curve. When cultured human skin fibroblast MAO was assayed along with haloperidol, MAO activity was only slightly affected (estimated IC50 = 3 X 10(-2) M), even with 1 hr of preincubation. When fibroblasts were cultured with medium containing haloperidol, however, the haloperidol IC50 for MAO activity was 3 X 10(-7) M after 3 days, 2 X 10(-8) M after 7 days, and 3 X 10(-9) M after 14 days. We conclude that haloperidol alters MAO enzyme activity acutely in vitro and that the inhibition increases at lower concentrations with chronic treatment in vivo.

Blood Platelets↗
PubMed1983

Back school. An overview with specific reference to the Canadian Back Education Units.

The Canadian Back Education Units (CBEU) in a review of 6418 participants found a significant subjective improvement in 69% of the participants. This figure improved to 80% when only patients who experienced back pain for six months or less were considered. Ninety-seven percent of the participants considered the back education program helpful. Patients who had completed their high school education, who believed that they understood the mechanism of the pain, and who recognized an emotional component to the problem had the best results. Functional improvement was most pronounced in the activities most often performed. Patients with pain persistently radiating below the knee and patients receiving workmen's compensation did not fare as well. Using a computer analysis of the variation in test scores from pretest to the review class, a statistically valid positive correlation was established between the patient's subjective improvement and the amount of information retained. The CBEU are an efficient, effective, well received, and cost-effective therapeutic modality in the conservative treatment of chronic low back pain.

Adult↗
PubMed1982

Cardiovascular and anticholinergic effects of zimelidine.

1. Pentobarbital anaesthetized mongrel dogs on artificial respiration were instrumented for recording of cardiovascular parameters. 2. Zimelidine or tricyclic antidepressants (amitriptyline, clomipramine or desipramine) were given i.v. at a rate of 0.5 mg/kg/min. 3. Zimelidine caused a moderate decrease in mean arterial blood pressure and in peripheral resistance. These effects were not dose dependent. 4. The tricyclic antidepressants induced a dose dependent decrease in mean arterial blood pressure and dose dependent increases in left ventricular enddiastolic pressure and in right atrial pressure. 5. It is concluded that the tricyclics have direct effects on the heart. Zimelidine has negligible direct heart effects but decreases peripheral resistance. 6. Studies in rat brain homogenates indicated very low affinity of zimelidine to muscarinic receptors. 7. Studies in mice indicated no central or peripheral anticholinergic effects of zimelidine in contrast to the tricyclics.

Amitriptyline↗
PubMed1981

Effects of antidepressant drugs on different receptors in the brain.

Radioligand receptor binding techniques were used to characterize the effects of different structural types of antidepressant drugs on neurotransmitter receptors. The tricyclic antidepressants more or less potently inhibited the binding to rat brain preparations of several different radiolabelled ligands [3H]WB4101, [3H]QNB, [3H]-d-LSD, [3H]mepyramine). The potency of the nontricyclic antidepressants varied greatly. Mianserin, potently displaced [3H]mepyramine, [3H]d-LSD and [3H]WB4101 while it was very weak on [3H]QNB-binding. Nomifensine and the specific 5-HT uptake inhibitors zimelidine and alaproclate had very low affinity for these receptors. All the antidepressants tested were practically devoid of activity on [3H]DHA binding, [3H]spiroperidol binding, [3H]flunitrazepam binding, [3H]muscimol binding and [3H]naloxone binding. The implications of these findings for biogenic amine theories of affective disorders are discussed.

Animals↗
PubMed1981

Binding affinity of levomepromazine and two of its major metabolites of central dopamine and alpha-adrenergic receptors in the rat.

N-Monodesmethyl levomepromazine and levomepromazine sulfoxide have previously been found in higher plasma concentrations than the parent drug in patients who received oral doses of levomepromazine. In the present study levomepromazine, N-monodesmethyl levomepromazine and levomepromazine sulfoxide have been assayed for their binding affinity to rat striatal dopamine receptors and to alpha-adrenergic receptors in rat cortex, and compared with the potency of chlorpromazine and some of its metabolites in the same systems. Levomepromazine sulfoxide was relatively inactive in the dopamine receptor binding test but much more active in the alpha-adrenergic receptor binding test, where it had a binding affinity similar to 7-hydroxy chlorpromazine. Levomepromazine and N-monodesmethyl levomepromazine were active in both systems, having a slightly higher potency than chlorpromazine in the alpha-adrenergic binding test, and a somewhat lower potency than chlorpromazine in the dopamine receptor binding test. The results indicate that N-monodesmethyl levomepromazine may significantly contribute to the antipsychotic effects of levomepromazine while the sulfoxide metabolite lacks neuroleptic potency, and that both metabolites may contribute to the autonomic side-effects of the drug.

Adrenergic alpha-Antagonists↗