Drugs online research references
J Pharmacol Exp Ther. 1983 Jan;224(1):80-8.
Differential-reinforcement-of-low-rate 72-second schedule: selective effects of antidepressant drugs.
O'Donnell JM, Seiden LS.
The effects of antidepressant drugs in rats responding under a differential-reinforcement-of-low-rate 72-sec schedule were assessed. Seven clinically used tricyclic antidepressant drugs (imipramine, desipramine, chlorimipramine, protriptyline, nortriptyline, amitriptyline and doxepin), two atypical antidepressants (iprindole and mianserin) and a monoamine oxidase inhibitor (tranylcypromine) dose-dependently reduced response rate and increased reinforcement rate. Nomifensine, an atypical antidepressant which has been reported to have psychomotor stimulant properties and abuse potential, increased response rate and decreased reinforcement rate. Chlorpromazine, an antipsychotic agent, and diphenhydramine, an antihistamine, have been reported to produce effects similar to antidepressants in several behavioral tests, but neither of these drugs mimicked the actions of antidepressants on responding under a differential-reinforcement-of-low-rate 72-sec schedule. Chlorpromazine decreased response rate but did not increase reinforcement rate. Diphenhydramine did not have consistent effects but tended to decrease reinforcement rate. These findings suggest that behavior maintained by the differential-reinforcement-of-low-rate schedule may be selectively affected by antidepressants that have no psychomotor stimulant properties.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6848751&dopt=Abstract
Chirality. 1991;3(1):14-8.
Comparative effects of the diastereoisomers, quinine and quinidine in producing phenocopy debrisoquine poor metabolisers (PMs) in healthy volunteers.
Ayesh R, Dawling S, Hayler A, Oates NS, Cholerton S, Widdop B, Idle JR, Smith RL.
Department of Pharmacology and Toxicology, St. Mary's Hospital Medical School, London, England.
1. A single oral dose (50 mg) of quinidine significantly increased the debrisoquine metabolic ratio in six healthy volunteers. For four of the volunteers the metabolic ratio changed to that typical of the poor metaboliser (PM) phenotype. 2. The effect of quinidine in producing debrisoquine oxidation "poor metaboliser" phenocopies persisted for at least 3 days but had disappeared by 1 week. 3. The debrisoquine metabolic ratios for the same six subjects were not significantly altered by the oral administration of quinine (200 or 400 mg), the diastereoisomer of quinidine. 4. The plasma pharmacokinetic parameters of both nortriptyline and desipramine in healthy volunteers were all changed to those more typical of the debrisoquine PM phenotype following the concomitant administration of quinidine (50 mg). 5. It is concluded that quinidine, but not its diastereoisomer quinine, is a potent selective inhibitor of the in vivo oxidation of debrisoquine and can produce an artifactual PM phenocopy in persons who are phenotypically extensive metaboliser (EM) phenotype status. The clinical implications of this observation are discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2039678&dopt=Abstract
Schweiz Med Wochenschr. 1982 Jul 24;112(30):1061-7.
[Drug hydroxylation disorders (debrisoquin type) in a random sample of the Swiss population]
[Article in German]
Dick B, Kupfer A, Molnar J, Braunschweig S, Preisig R.
The hydroxylation phenotype was determined in a sample of the Swiss population consisting of 222 normal unrelated subjects (131 women, 91 men). Following oral administration of a single dose of 19 mg debrisoquine, urine was collected for 8 hours. Urinary concentrations of parent compound and its major metabolite (4-hydroxydebrisoquine) were measured with GLC and their molar ratio ("metabolic ratio", MR) was calculated and plotted as a frequency distribution histogram. The frequency distribution of the MR was clearly bimodal, exhibiting two clusters of MR's of 0.1 to 1.0 and 20 to 100, respectively. Using probit analysis, the antimode was found at an MR of 12.6 Consequently, 22 subjects (16 women, 6 men), representing 10% of the population studied, were, with an MR of greater than 12.6, considered to be poor hydroxylators (PM). The families of two subjects, established as PMs in the population study, were also investigated. One family was found to be the first known pairing of homozygous PM parents with all 6 offspring exhibiting the PM phenotype. In both families the pattern was consistent with an autosomal recessive mode of inheritance for the two alleles E (extensive) and N (none) respectively. Clinical consequences of the PM phenotype known to date are summarized. Since some drugs typically used for longterm treatment (such as perhexiline, phenytoin, nortriptyline, guanoxan) are subject to the same hydroxylation pathway, PM patients are likely to be at higher risk of drug toxicity. This relationship has been well documented for perhexiline-induced neuropathy. Conversely, it is conceivable that with the use of prodrugs which have to be hydroxylated to the active compound, PM subjects might turn out to be "non-responders".
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7123181&dopt=Abstract
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