Drugs online research references
Br J Pharmacol. 1998 Jun;124(4):669-74.
The involvement of the opioidergic system in the antinociceptive mechanism of action of antidepressant compounds.
Gray AM, Spencer PS, Sewell RD.
Division of Pharmacology, The Welsh School of Pharmacy, UWC, Cardiff, Wales.
1. Debate exists as to the nature of antidepressant-induced antinociception. It is unclear whether antidepressants are inherently antinociceptive, are able to potentiate opioid antinociception or both. We have used the acetic acid induced abdominal constriction assay in mice to investigate antidepressant-induced antinociception. 2. All the antidepressants tested (s.c.) produced dose-dependent protection against acetic acid-induced abdominal constriction. Similarly, morphine and aspirin were also effective antinociceptive agents in this nociceptive assay. 3. Opioid antagonists, naloxone (0.5 mg kg(-1), s.c.) and naltrindole (1 mg kg(-1), s.c.), shifted the dose-response relationships to the right for each of the antidepressant agents (dothiepin, amitriptyline, sibutramine, (+)-oxaprotiline and paroxetine). In this context the naloxone dose-ratios were 1.95, 3.90, 2.32, 4.50 and 2.65, with naltrindole dose-ratios of 4.36, 17.00, 4.28, 11.48 and 2.65 were obtained, respectively. Naloxone also shifted the morphine dose-response relationship to the right, by a factor of 2.62, whilst naltrindole had no effect upon morphine antinociception. Aspirin antinociception remained unaffected by both opioid antagonists. 4. The enkephalin catabolism inhibitor acetorphan, by itself, produced no activity in this test at a dose of 10 mg kg(-1) (s.c.). However, at higher doses, acetorphan produced a linear dose-response relationship against acetic acid-induced abdominal constriction. 5. When acetorphan was administered before either the antidepressants or morphine, there was a clear potentiation of the antidepressant- or morphine-induced antinociception. However, acetorphan had no effect on aspirin antinociception. 6. Since neither of the opioid antagonists were able to attenuate, nor was acetorphan able to potentiate, aspirin antinociception, we concluded that the mechanism of antidepressant-induced antinociception is different from that of the non-steroidal anti-inflammatory drugs. 7. These data are consistent with the view that antidepressants may induce endogenous opioid peptide release, as shown by the acetorphan study. In this context, the ability of naltrindole to displace the antidepressant dose-response relationship to the right without affecting morphine antinociception, implicates the delta-opioid receptor and endogenous opioid peptides in antidepressant-induced antinociception.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9690858&dopt=Abstract
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J Pharm Biomed Anal. 1995 Apr;13(4-5):635-8.
A simple and robust HPLC method for the determination of paroxetine in human plasma.
Knoeller J, Vogt-Schenkel R, Brett MA.
Focus Clinical Drug Development GmbH, Neuss, Germany.
The objective of this investigation was to establish and validate an HPLC method with UV detection for the determination of paroxetine in human plasma. The method was validated in the concentration range from 6 to 100 ng ml-1. The lower limit of reliable quantification (LLQ) was 6 ng ml-1. The extraction efficiency varied from 67.1 to 85.5% over this range. Accuracies calculated at three concentrations in each of three separate runs were between 99.4 and 109.6%, and precision data were between 1.86 and 9.1%. The means of the between-day precision at all concentrations were between 2.77 and 7.32%. The corresponding means of the accuracy data were in the region of 102.4 to 106.3%.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9696579&dopt=Abstract
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Biol Psychiatry. 1998 Aug 15;44(4):274-80.
Biological parameters in major depression: effects of paroxetine, viloxazine, moclobemide, and electroconvulsive therapy. Relation to early clinical outcome.
Lestra C, d'Amato T, Ghaemmaghami C, Perret-Liaudet A, Broyer M, Renaud B, Dalery J, Chamba G.
Laboratoire de Biochimie, Hopital Neurologique, Lyon, France.
BACKGROUND: Clinical and pharmacologic studies report a relative or absolute serotonergic deficiency in major depression; however, the variability of clinical characteristics of illness has led to controversial results. In the present work, we looked for a possible relationship between i) biochemical values that indirectly reflect aminergic neurons activity and clinical characteristics and ii) their evolution and the early clinical outcome under antidepressive therapies (ATs). METHODS: Platelet serotonin content, platelet monoamine oxydase activity, and urinary biopterins were measured in 27 depressed patients before and during four different ATs (paroxetine, viloxazine, moclobemide, or electroconvulsive therapy). Depressive symptomatology and its evolution under ATs were quantified using three clinical rating scales. RESULTS: A severe symptomatology, high serotonin (5-HT) platelet content, and high or low urinary B could represent risk factors leading to a smaller or delayed response to an AT. Furthermore, the early improvement under ATs was negatively correlated to pretreatment 5-HT platelet content. CONCLUSIONS: Determination of 5-HT level could be useful in the choice of an AT.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9715359&dopt=Abstract
note: kwd match paxil online literature
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