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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 718 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 35 (1992), S. 163-169 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine and other mediators have been shown to be involved in the ethanol-induced jejunal plasma protein loss. In this study we have investigated whether the histamine (H)-related component of this protein loss is mediated by H1-receptors, H2-receptors or both. Four groups of dogs (n=12 in each) were studied. They were: untreated, H1+H2-receptor blockade, H1-receptor blockade and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptors respectively. In all animals, jejunal protein loss was measured over 10 min periods for 90 min. Ethanol increased protein loss in all time periods (p〈0.001). This protein loss was depressed by H1+H2-receptors blockade throughout 90 min (p〈0.01). H1-receptor blockade caused a similar depression of ethanol effect but only during 20 to 40 min (p〈0.05). In contrast, H2-receptor blockade aggravated the protein losing effect of ethanol throughout 90 min (p〈0.01). Analyses of data tend to suggest that the ethanol-induced protein loss is mediated principally by H1-receptors, and that a complete inhibition of the histamine-related ethanol-induced protein loss can be achieved only by a simultaneous blockade of both H1 and H2- receptors, and not by H1- or H2-receptor blockade alone.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 795-802 
    ISSN: 1573-2568
    Keywords: chest pain ; Holter electrocardiography ; esophageal dysmotility ; gastroesophageal reflux
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Standard Holter electrocardiographic (ECG) monitoring was combined with ambulatory esophageal manometry and pH-metry in 25 patients with atypical chest pain in order to determine whether an association could be found between spontaneous pain episodes and ischemic ECG changes or esophageal dysfunction. Results of ambulatory testing were compared to those obtained with standard esophaeal manometry and provocative testing. Twenty-two of the 25 patients experienced a total of 88 pain episodes during ambulatory testing. Although 15 of the 22 patients (68%) experiencing pain during testing had at least one pain episode that corelated temporally with gastroesophageal reflux, esophageal dysmotility or ischemic ECG changes, 65% of all pain episodes were unrelated to abnormal esophageal events or ECG changes. Seventeen percent of pain episodes were associated with gastroesophageal reflux, 15% with esophageal dysmotility,and 2% with a combined acid reflux and esophageal dysmotility event. Only one pain episode was associated with ischemic ECG changes. Twelve of the 15 patients with chest pain episodes associated with reflux or esophageal dysmotility had othe identical pain episodes in which there was no correlation. Reproduction of a patient's pain during standard manometry with provocative testing did not predict a strong correlation between the patient's spontaneous pain episodes and esophageal dysfunction during ambulatory recordings. In summary, patients with atypical chest pain have relatively few spontaneous pain episodes that correlate with gastroesophageal reflux, esophageal dysmotility, or ischemic ECG changes. It appears that different stimuli can trigger identical episodes of chest pain, which suggests that many of these patients may have dysfunction of their visceral pain sensory mechanisms.
    Type of Medium: Electronic Resource
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