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  • Electronic Resource  (3)
  • 1995-1999  (3)
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  • Electronic Resource  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 16 (1998), S. 0 
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 105 (1996), S. 10224-10236 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: The intermolecular vibrational energy levels supported by the OH A 2Σ+ (v′=0,1)+N2 potentials have been characterized spectroscopically through excitation of OH–N2 complexes in the OH A 2Σ+–X 2Π 0–0 and 1–0 spectral regions. At least 95 levels correlating with OH A 2Σ+ (v′=0)+N2 are observed in fluorescence depletion experiments. OH–N2 complexes prepared in these levels have lifetimes with lower limits ranging from 1.4 to 8 ps due to rapid electronic quenching which precludes their detection by laser-induced fluorescence. An onset of OH–N2 laser-induced fluorescence occurs at the OH A 2Σ+ (v′=0)+N2 dissociation limit, enabling determination of the ground and excited state binding energies at ∼250 and ≥1372 cm−1, respectively. In the OH A–X 1–0 region, OH–N2 transitions originating from a common ground state level to single or groups of intermolecular vibrational levels correlating with OH A 2Σ+ (v′=1)+N2 are observed via laser-induced fluorescence and fluorescence depletion measurements. Comparison of the OH–N2 spectra obtained in the OH A–X 0–0 and 1–0 regions reveals that vibrational excitation of OH A 2Σ+ increases the OH–N2 binding energy by 139 cm−1. OH–N2 complexes excited in the OH A–X 1–0 region undergo ultrafast dynamics (〈200 fs) which give rise to extensive spectral line broadening. A kinetic model indicates that vibrational predissociation is the dominant decay channel for OH–N2 prepared in the intermolecular levels derived from OH A 2Σ+ (v′=1)+N2. © 1996 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1041
    Keywords: Key words Moexipril ; Hydrochlorothiazide; pharmacokinetics ; drug interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: To investigate the potential for pharmacokinetic interactions between moexipril, a new converting enzyme inhibitor, and hydrochlorothiazide after single dose administration. Methods: 12 healthy male volunteers were studied by an open, randomised, three-way cross-over design, in which single doses of moexipril, hydrochlorothiazide and the two drugs together were administered. Blood and urine were collected up to 48 hours for measurement of the concentrations of moexipril and its metabolite moexiprilat. In addition, the urine samples were analysed for hydrochlorothiazide. Results: For the area under the plasma concentration-time curve calculated from time 0 to a concentration greater than zero, AUC(0–t), the study showed a mean value of moexipril 437 ng ⋅ ml−1⋅ h−1 following administration of moexipril alone and 416 ng ⋅ ml−1⋅ h−1 following moexipril concomitantly with hydrochloro- thiazide. The corresponding values for the metabolite moexiprilat were 203 and 215 ng ⋅ ml−1⋅ h−1, respectively. The cmax of moexipril and the metabolite (data of the metabolite in parenthesis) were 245.4 (70.8) ng ⋅ ml−1 after administration of moexipril alone and 241.0 (69.2) ng ⋅ ml−1 after coadministration of hydrochlorothiazide. The mean total renal excretion (TUE) of hydrochlorothiazide was 15.2 mg when administered alone and 15.1 mg when given together with moexipril. The corresponding mean TUE-values for moexiprilat were 334 (1200) and 453 (1460) μg. Conclusion: The coadministration of moexipril with hydrochlorothiazide had no demonstrable effect on the measured pharmacokinetic parameters of moexipril, its active metabolite moexiprilat or hydrochlorothiazide.
    Type of Medium: Electronic Resource
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