Ambien online research references
Zh Nevrol Psikhiatr Im S S Korsakova. 1999;99(12):40-2.
[Treatment of insomnia in patients with borderline mental diseases]
[Article in Russian]
Tsivil'ko MA, Korkina MV, Shinaev NN, Volkova NP, Kucherov AIu.
Zolpidem, non-benzodiazipine preparation, was used for therapy of 56 patients with insomnia. 4 groups of patients were treated: a) with a prevalence of asthenic symptomatology in psychogenic disorders; b) with polymorphic neurotic symptomatology and autonomic disorders; c) with affective pathology of neurotic level; d) with nervous anorexia and bulimia. Zolpidem was quite effective in all groups of patients in terms of normalization of falling asleep, improvement of quality of sleep without changing of daily activity. A good drug tolerance was found in elderly patients.
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J Chromatogr B Biomed Sci Appl. 1997 Jul 4;694(2):409-13.
Rapid and simple method for the determination of zolpidem in human plasma by high-performance liquid chromatography.
Ptacek P, Macek J, Klima J.
Pharmakl s.r.o., U vojenske nemocnice, Prague, Czech Republic.
A simple and reproducible method for the determination of zolpidem in human plasma is presented. This method involves protein precipitation with methanol (2 ml of methanol are added to 0.5 ml of plasma) and reversed-phase chromatography with fluorescence detection (excitation wavelength 244 nm, emission wavelength 388 nm). The mobile phase consists of methanol-30 mM dihydrogen potassium phosphate-triethylamine (30:69:1). pH of the aqueous part of the mobile phase is 6.8. No internal standard is required. Limit of quantitation is 1.5 ng/ml and the calibration curve is linear up to 400 ng/ml. Within-day and between-day precision expressed by relative standard deviation is less than 5% and inaccuracy also does not exceed 9%. The assay is useful for pharmacokinetic studies.
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Neuroscience. 1997 Oct;80(4):1101-11.
Shortened-duration GABA(A) receptor-mediated synaptic potentials underlie enhanced CA1 excitability in a chronic model of temporal lobe epilepsy.
Mangan PS, Bertram EH 3rd.
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, U.S.A.
Intracellular recording techniques were used to examine GABA(A) receptor-mediated synaptic inhibition in pyramidal cells of the CA1 region of the rat hippocampus in the post-self sustaining limbic status epilepticus model of temporal lobe epilepsy. Orthodromically evoked, monosynaptic inhibitory postsynaptic potentials were recorded in vitro following pharmacological blockade of ionotropic glutamate and GABA(B) receptors. Inhibitory postsynaptic potentials from epileptic tissue were kinetically altered relative to controls; both the 10-90% rise-time and width (measured at half-maximum amplitude) were reduced by approximately 50% resulting in significant shortening of duration. The degree of pyramidal cell hyperexcitability, assessed before pharmacological treatment as the number of action potentials evoked by maximum intensity afferent stimulation, correlated significantly with the magnitude of synaptic potential duration reduction determined following blockade of glutamatergic neurotransmission. Bath application of the benzodiazepine type 1 receptor agonist zolpidem reduced post-self sustaining limbic status epilepticus CA1 pyramidal cell hyperexcitability substantially (but not completely) via a marked increase in inhibitory postsynaptic potential area. Post-self-sustaining limbic status epilepticus inhibitory postsynaptic potentials which exhibited the most pronounced shortening were augmented by zolpidem to a greater degree than longer duration synaptic potentials. In contrast, zolpidem-induced augmentation of control inhibitor, postsynaptic potential area was much less robust. It is suggested that a deficiency in post-self-sustaining limbic status epilepticus GABA(A) receptor-mediated synaptic inhibition contributes to a state of partial disinhibition which is a major factor in enhanced CA1 excitability in chronic limbic epilepsy. Possible mechanisms underlying post-self-sustaining limbic status epilepticus kinetic abnormalities are discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9284063&dopt=Abstract
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J Anal Toxicol. 1997 Sep;21(5):388-92.
Analysis of zolpidem in human plasma by high-performance liquid chromatography with fluorescence detection: application to single-dose pharmacokinetic studies.
Durol AL, Greenblatt DJ.
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA 02111, USA.
Zolpidem, an imidazopyradine hypnotic agent, can be quantitated by high-performance liquid chromatography (HPLC) with fluorescence detection. After the addition of a structurally related internal standard (propyl-zolpidem), plasma samples were double-extracted at neutral pH with toluene-isoamyl alcohol or benzene-isoamyl alcohol. The organic extracts were evaporated to dryness, reconstituted with mobile phase, and analyzed by HPLC using a C-18 reversed-phase column, a mobile phase of acetonitrile-50mM potassium dihydrogen phosphate (50:50), and fluorescence detection with excitation and emission wavelengths of 254 and 390 nm, respectively. The lower limit of reliable quantitation was in the range of 1-2.5 ng/mL. The method is applicable to single-dose pharmacokinetic studies of zolpidem in humans.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9288593&dopt=Abstract
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J Med Chem. 1997 Sep 12;40(19):3109-18.
Synthesis and binding affinity of 2-phenylimidazo[1,2-alpha]pyridine derivatives for both central and peripheral benzodiazepine receptors. A new series of high-affinity and selective ligands for the peripheral type.
Trapani G, Franco M, Ricciardi L, Latrofa A, Genchi G, Sanna E, Tuveri F, Cagetti E, Biggio G, Liso G.
Dipartimento Farmaco-Chimico and Farmaco-Biologico, Facolta di Farmacia, Universita degli Studi di Bari, Italy.
A number of 6-substituted or 6,8-disubstituted alkyl 2-phenylimidazo[1,2-alpha]pyridine-3-carboxylates 5a-h, -acetates 5i-s, 6a-g, and -propionates 5t, 6h and of N,N-dialkyl-2-phenylimidazo[1,2-alpha]pyridine-3-carboxamides 7a-d,-acetamides 7e-t or -propionamide 7u were prepared following new synthetic methods, and their affinities for both the central (CBR) and the peripheral (PBR) benzodiazepine receptors evaluated. The compounds of the ester series displayed low affinity for both receptor types. Conversely, most of N,N-dialkyl(2-phenylimidazo[1,2-alpha]pyridin-3-yl)acetamides 7e-t proved to possess high affinity and selectivity for CBR or PBR depending on the nature of substituents at C(6)- and/or C(8) on the heterocyclic ring system. In particular, the 6-substituted compounds 7f-n displayed ratios of IC50 values (IC50(CBR)/IC50(PBR)) ranging from 0.32 (7m) to 232 (7k), while the 6,8-disubstituted compounds 7o-t were more than 1000-fold more selective for PBR versus CBR. Compounds 7f,m were examined in several different benzodiazepine receptor subtypes. Expression of specific GABAA, receptor subunit assemblies in Xenopus oocytes was utilized to evaluate functionally both the efficacy and potency of the positive modulation of GABA-evoked Cl- currents by 7f and 7m in comparison with Zolpidem. The rank order of potencies of these drugs was 7f (EC50 = 3.2 x 10(-8) M) > Zolpidem (EC50 = 3.6 x 10(-8) M) > 7m (EC50 = 2.2 x 10(-7) M). The actions of these compounds were also tested on alpha 2 beta 2 gamma 2s, receptors. However, the EC50 of these compounds was increased, compared to alpha 1 beta 2 gamma 2s receptors, by 30-, 4-, and 5-fold for 7m, 7f, and Zolpidem, respectively. Finally, these compounds were almost completely devoid of activity at receptors containing the alpha 5 subunit.
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