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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 187 (1987), S. 303-313 
    ISSN: 1433-8580
    Keywords: Carrageenin oedema ; Immobilisation stress ; Noradrenaline ; Adrenal gland ; Sympathetic system ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of immobilisation stress on acute pedal inflammation induced by carrageenin, and the mechanism of stress-induced anti-inflammatory effect, were investigated in male Wistar strain albino rats. Carrageenin-induced pedal inflammation oedema was attenuated by immobilisation stress in a time-dependent manner, when the rats were restrained for 30 min, 1 h, and 2 h immediately after the induction of the inflammation. Pentobarbitone exhibited significant anti-inflammatory effect of its own in an anaesthetic dose and also inhibited stress (1 h)-induced attenuation of the inflammation. Likewise, lignocaine, injected behind the knee joint of the inflamed limb, attenuated the inflammation and also inhibited the stressinduced anti-inflammatory effect. These findings indicate the importance of the central nervous system (CNS) and the afferent/efferent neural pathways from and to the inflammatory site, in inflammation and in stress-induced anti-inflammatory effect. Earlier studies from this laboratory have shown that the central noradrenergic, histaminergic, serotonergic and GABA-ergic neurotransmitter systems have a modulatory anti-inflammatory effect on carrageenin-induced pedal oedema. Since all these neurotransmitter systems have been reported to be activated by stress, their role was assessed in the inflammation-attenuation effect of immobilisation stress. The present studies indicate that, of these neurotransmitters, only the central noradrenergic system is involved in the anti-oedema effect of stress. Endogenous opioid peptides may also be involved in the stress-inflammation interaction, since naloxone inhibited the stress effect. Bilateral adrenalectomy and peripheral chemical sympathectomy, induced by i.p. administration of 6-hydroxydopamine, augmented carrageenin oedema and antagonised the stress-induced anti-inflammatory effect. However, metyrapone, an inhibitor of endogenous corticoid synthesis, failed to inhibit the stress effect. These findings indicate that the sympatho-medullary system, which is known to be activated during stress, is responsible for the observed anti-inflammatory effect of immobilisation stress, rather than augmented release of adrenal corticoids. It is suggested that the observed inflammation reducing effect of immobilisation stress is a consequence of increased central noradrenergic and peripheral sympatho-medullary activity.
    Type of Medium: Electronic Resource
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  • 2
    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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