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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 17 (1985), S. 150-152 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intracerebroventricularly (icv) administered histamine (5, 10 and 20 μg) produced a dose-related anti-inflammatory effect against carrageenin-induced pedal edema in rats. The effect of histamine was mimicked by the H1 receptor agonist, 2-methylhistamine, but not by the H2 receptor agonist, 2-methylhistamine, The anti-inflammatory effect of centrally administered histamine was antagonised by mepyramine, a H1 receptor antagonist, but not by cimetidine, a H2 receptor antagonist. The anti-inflammatory effect of icv histamine was inhibited in bilaterally adrenalectomised rats but was unaffected by peripheral chemical sympathectomy induced by 6-hydroxydopamine.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 2 (1985), S. 137-139 
    ISSN: 1573-904X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Possible central cholinergic modulation of acute peripheral inflammation was investigated in rats, adopting the carrageenin-induced acute pedal edema as the experimental model. Intracerebroventricularly (icv) administered acetylcholine (Ach) and tremorine, a central cholinomimetic agent, significantly augmented the inflammation, whereas hemicholinium, which inhibits Ach synthesis, attenuated the edema. Paradoxically, icv administered atropine sulphate induced an Ach like pro-inflammatory effect and also failed to affect the Ach action. The atropine-induced inflammation promoting effect was annulled after hemicholinium pre-treatment, suggesting that it was dependent on the integrity of central cholinergic function. The pro-inflammatory effect of icv Ach was negated after peripheral administration of atropine ethoiodide. It is suggested that the carrageenin inflammation promoting effect of centrally administered Ach is due to enhanced peripheral cholinergic activity.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 186 (1986), S. 365-374 
    ISSN: 1433-8580
    Keywords: Carrageenin oedema ; Noradrenaline ; Dopamine ; Central modulation of inflammation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricularly (i.c.v.) administered noradrenaline (NA) andl-dopa, but not dopamine (DA), attenuated carrageenin-induced pedal oedema in rats. Centrally administered reserpine and the catecholaminergic neurotoxin, 6-hydroxydopamine (6-HD), augmented the inflammatory oedema. Pharmacological treatments, which selectively increase central DA, induce DA neurone degeneration and affect DA receptor activity, were singularly ineffective in modifying the inflammatory response of carrageenin. Centrally administered phentolamine, an α-adrenergic receptor antagonist, produced a dose-related dual effect on the peripheral oedema. Lower doses of phentolamine produced a paradoxical NA-like oedema-attenuating effect, which was not evident in 6-HD-treated rats; however, a larger dose of the drug had no per se effect but antagonised the oedema-inhibiting effect of centrally administered NA. Propranolol, a β-adrenergic receptor antagonist produced inconsistent effects, with a lower and higher dose of the drug showing no effect, while a median dose induced an inhibitory effect on the peripheral oedema. Bilateral adrenalectomy failed to antagonise the anti-inflammatory effect of central NA, but peripheral degeneration of sympathetic neurones, induced by i.p. administered 6-HD, inhibited the effect of NA. The results of the study indicate that central NA, but not DA, exerts a modulatory inhibitory effect on peripheral oedema induced by carrageenin. This effect of central NA appears to be dependent upon the peripheral sympathetic system and not on the activation of the adrenal corticoid activity.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 2 (1985), S. 315-318 
    ISSN: 1573-904X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Putative central serotonergic modulation of acute peripheral inflammation was investigated in rats, using the carrageenin-induced pedal edema as the experimental model. Serotonin and the serotonin precursor 5-hydroxytryptophan (5HTP) produced a dose-related inhibition of the peripheral edema when given intracerebroventricularly (icv) and ip, together with the peripheral decarboxylase inhibitor benserazide. Quipazine, which inhibits neuronal release of serotonin, 5,6-dihydroxytryptamine (DHT), a specific serotonergic neurotoxin, and p-chlorphenylalanine, a selective serotonin synthesis inhibitor, augmented carrageenin inflammation upon icv administration. Metergoline, a serotonin receptor antagonist, inhibited the anti-inflammatory effect of centrally administered serotonin. However, another serotonin receptor antagonist, methysergide, produced a serotonin-like effect. The inflammation-inhibiting effect of centrally administered methysergide was antagonized after DHT-pretreatment. The findings indicate that in rats central serotonin has a modulatory inhibitory effect on acute peripheral inflammation. It was further shown that this inhibitory effect is not mediated either through activation of the peripheral sympathetic nervous system or the adrenal cortex.
    Type of Medium: Electronic Resource
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