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  • 1
    Electronic Resource
    Electronic Resource
    Lack of interaction of ranitidine with amitriptyline (1987)
    Springer
    European journal of clinical pharmacology 32 (1987), S. 317-320 
    Details
    ISSN: 1432-1041
    Keywords: ranitidine ; amitriptyline ; drug interaction ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The possibility of an interaction of ranitidine with amitriptyline was assessed by means of amitriptyline and nortriptyline plasma concentration measurements, blood pressure and pulse rate, digit symbol substitution, and visual analogue scales. Ranitidine had no effect on amitriptyline or nortriptyline concentrations. Responses recorded by the digit symbol substitution and visual analogue scale tests correlated with changes in concentrations of amitriptyline and nortriptyline in plasma. No effects on blood pressure or pulse rate were observed. We concluded that there was no effect of ranitidine on amitriptyline kinetics or response in the conditions of our study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00607582
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Cimetidine interaction with amitriptyline (1985)
    Springer
    European journal of clinical pharmacology 29 (1985), S. 429-433 
    Details
    ISSN: 1432-1041
    Keywords: amitriptyline ; cimetidine ; pharmacokinetic interaction ; psychomotor skills ; cardiovascular effects ; nortriptyline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The interaction of cimetidine with amitriptyline was assessed by means of amitriptyline and nortriptyline plasma concentration measurements, standing blood pressure and pulse rate, digit symbol substitution, and visual analogue scales. Cimetidine increased plasma amitriptyline concentrations and decreased plasma nortriptyline concentrations, apparently by inhibiting presystemic metabolism. The changes in blood pressure, pulse rate and digit symbol substitution correlated with changes in concentrations of amitriptyline in plasma and expected changes based on a dose ranging preliminary experiment. Changes in subjective ratings of effects correlated with changes in nortriptyline concentrations in plasma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00613457
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Review article: diagnosis and management of night-time reflux (2004)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 20 (2004), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Symptoms of gastro-oesophageal reflux disease (GERD) range from mild to severe and, when they occur during night-time hours, can interfere with sleep patterns and reduce overall quality of life. The clinical presentation of GERD is characterized by oesophageal as well as supra-oesophageal symptoms, including otolaryngologic and pulmonary complications. However, GERD may be overlooked as the cause of a patient's supra-oesophageal symptoms because these complaints can occur in the absence of oesophageal symptoms or endoscopic changes. The role of available tools used for GERD diagnosis, including endoscopy, oesophageal pH monitoring and an empirical course of proton pump inhibitor therapy, is discussed. Interventions available to achieve the therapeutic goals of symptom relief and prevention include specific lifestyle modifications and over-the-counter as well as prescription pharmacological agents. Patient-initiated, as-needed treatment may not be the best choice for managing persistent night-time reflux because it requires patient arousal from sleep. Proton pump inhibitor therapy remains the treatment of choice for patients with more severe symptoms and those with erosive oesophagitis. Few studies have specifically evaluated the role of pharmacological agents in the management of night-time reflux and comparisons are difficult due to the variability in study design and endpoints assessed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.02241.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Functional and anatomical relationships between antral gastrin cells and gastrin-releasing peptide neurons (1985)
    Springer
    Histochemistry and cell biology 82 (1985), S. 463-467 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The present studies were directed to examine the effect of gastrin-releasing peptide (GRP) on β-adrenergic stimulated gastrin release by cultured rat antral mucosa and to assess the anatomical relationship between gastrin cells and GRP nerves in rat and human antrum. Peptide-containing cells were identified by application of an avidinbiotin-peroxidase immunocytochemical double staining method utilizing antibodies to GRP and gastrin prepared in rabbits. Rat antral mucosa was cultured for 60 min and gastrin released into the culture medium was measured by radioimmunoassay. Inclusion of antibodies to GRP in culture medium did not affect carbachol-stimulated gastrin release, whereas isoproterenol-stimulated gastrin release into the medium was inhibited significantly by addition of GRP antiserum to the culture medium. GRP-containing neurons and axonal fibers were stained immunocytochemically with diaminobenzidine (reddish-brown specific staining) and were located in the lamina propria adjacent to and surrounding the main lobules of antral glands. After double staining utilizing 4-Cl-1-Naphthol as substrate, blue stained gastrin-containing cells were identified in the middle and deeper regions of antral glands in close proximity to GRP neuronal elements. These studies suggest that β-adrenergic, but not cholinergic, stimulation of gastrin release is mediated, at least in part, through GRP. They also demonstrate intimate anatomical, as well as functional, relationships between gastrin cells and GRP-containing neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02450481
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    Paper (German National Licenses)
    Fulltext
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