Inhibition of carrageenin-induced pedal oedema in rats by immobilisation stress.
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 stress-induced 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.
D015115:5,6-Dihydroxytryptamine / Q000627:therapeutic use; D000315:Adrenalectomy; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002351:Carrageenan / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D004487:Edema / Q000139:chemically induced* / Q000503:physiopathology; D005534:Foot Diseases / Q000139:chemically induced* / Q000503:physiopathology; D006892:Hydroxydopamines / Q000627:therapeutic use; D007103:Immobilization; D007249:Inflammation / Q000139:chemically induced*; D008297:Male; D016627:Oxidopamine; D010424:Pentobarbital / Q000627:therapeutic use; D051381:Rats; D011919:Rats, Inbred Strains; D013312:Stress, Physiological
D000893:Anti-Inflammatory Agents; D006892:Hydroxydopamines; D016627:Oxidopamine; D002351:Carrageenan; D010424:Pentobarbital; D015115:5,6-Dihydroxytryptamine