Drugs online research references
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The aim of this study was to investigate the effect of three selective serotonin reuptake inhibitors (SSRIs), fluoxetine, fluvoxamine and sertraline, on the pharmacokinetics and metabolism of perazine in a steady state in rats. Perazine (10 mg kg(-1), i.p.) was administered twice daily for two weeks, alone or jointly with one of the SSRIs. Concentrations of perazine and its two main metabolites (N-desmethylperazine and 5-sulfoxide) in the plasma and brain were measured 30 min and 6 and 12 h after the last dose of the drugs. Of the investigated SSRIs, fluoxetine and fluvoxamine significantly increased plasma and brain concentrations of perazine (up to 900% and 760% of the control value, respectively), their effect being most pronounced after 30 min and 6 h. Moreover, simultaneous increases in perazine metabolites concentrations and in the perazine/metabolite concentration ratios were observed. Sertraline elevated plasma and brain concentrations of perazine after 30 min. In-vitro studies with liver microsomes of rats treated chronically with perazine, SSRIs ortheir combinations showed decreased concentrations of cytochrome P-450 after perazine and a combination of perazine and fluvoxamine (vs control), and increased concentration after a combination of perazine and fluoxetine (vs perazine-treated group). Prolonged treatment with perazine did not significantly change the rate of its own metabolism. Chronic administration of fluoxetine or sertraline, alone or in a combination with perazine, accelerated perazine N-demethylation (vs control or perazine group, respectively). Fluvoxamine had a similar effect. The 5-sulfoxidation of perazine was accelerated by fluvoxamine and sertraline treatment, but the process was inhibited by administration of a combination of perazine and fluoxetine or fluvoxamine (vs control). Kinetic studies using control liver microsomes, in the absence or presence of SSRIs added in-vitro, demonstrated competitive inhibition of both N-demethylation and sulfoxidation by the investigated SSRIs. Sertraline was the most potent inhibitor of perazine N-demethylation but the weakest inhibitor of sulfoxidation. Results of in-vivo and in-vitro studies indicate that the observed interaction between perazine and SSRIs mainly involves competition for an active site of perazine N-demethylase and sulfoxidase. Moreover, increases in the concentrations of both perazine and metabolites measured, produced by the investigated drug combinations in-vivo, suggest simultaneous inhibition of another, yet to be investigated, metabolic pathway of perazine (e.g. aromatic hydroxylation).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11341361&dopt=Abstract
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Fresenius J Anal Chem. 2001 Apr;369(7-8):563-6.
Electrochemical behaviour of sertraline at a hanging mercury drop electrode and its determination in pharmaceutical products.
Vela MH, Quinaz Garcia MB, Montenegro MC.
CEQUP/Departamento de Quimica-Fisica, Faculdade de Farmacia, Universidade do Porto, Portugal.
The electrochemical behaviour of sertraline at a hanging mercury drop electrode (HMDE) was described. Different voltammetric techniques, such as cyclic, linear sweep, differential pulse and square wave voltammetry, were used. Voltammograms were obtained at different pH values with a Britton-Robinson buffer solution used as supporting electrolyte. The best results were found by square wave voltammetry with electrodeposition at alkaline pH using a borate buffer with a pH = 8.2 for the samples, containing 12% (v/v) methanol. Under optimised conditions, a linear relationship between 2.33 x 10(-7) and 3.15 x 10(-6) M of sertraline with a limit of detection of 1.98 x 10(-7) M was obtained. The electrochemical method developed was applied to the determination of sertraline in pharmaceutical formulations. Recoveries were close to 100%, thus proving efficacy of the proposed method for the quantification of sertraline in commercial samples.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11371048&dopt=Abstract
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J Urol. 2001 Jun;165(6 Pt 1):2110-4.
Comparison of peripheral inhibitory effects of clomipramine with selective serotonin re-uptake inhibitors on contraction of vas deferens: in vitro and in vivo studies.
Seo KK, Kim SC, Lee MY.
Department of Urology and Physiology, College of Medicine, Chung-Ang University, Seoul, Korea.
PURPOSE: We compared the peripheral inhibitory effects of the tricyclic antidepressant clomipramine with those of various selective serotonin re-uptake inhibitors on the contractile response of the vas deferens. MATERIALS AND METHODS: The contractile responses of 17 circular smooth muscle strips of human vas deferens to 10-4 M. norepinephrine were observed in the absence and presence of clomipramine, and the selective serotonin re-uptake inhibitors fluoxetine, sertraline and paroxetine. The intraluminal pressure response of rat vas deferens to electrical stimulation of the hypogastric nerve was measured in 5 rats in the central plus peripheral effect group before and after the intravenous injection of 4.2 mg./kg. clomipramine or 8.3 mg./kg. sertraline. The pressure response to each agent was also observed after the transection of all proximal sympathetic input to the hypogastric nerve in 5 animals in the peripheral effect group. RESULTS: Clomipramine was about 100-fold more potent than sertraline, fluoxetine or paroxetine for inhibiting the norepinephrine induced contraction of human vasal muscle strips. The inhibitory effect of sertraline on rat intravasal pressure in the peripheral effect group was significantly lower than in the central plus peripheral effect group (p <0.05), while no significant difference was noted in the 2 groups regarding clomipramine. The effect of clomipramine was significantly higher than that of sertraline in the central plus peripheral and peripheral effect groups (p <0.01). CONCLUSIONS: Differences in potency of the peripheral inhibitory effects of the selective serotonin re-uptake inhibitors and clomipramine may contribute to their differential effects on delaying ejaculatory latency in patients with premature ejaculation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11371937&dopt=Abstract
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