Inhibition of carrageenin-induced pedal oedema in rats by immobilisation stress

Abstract

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.

Repeated, but not acute, stress suppresses inflammatory plasma extravasation

“…Earlier reports have indicated that acute stress can inhibit plasma extravasation if the inflammatory challenge is presented during the stressful stimulus (10,11). However, the inhibition of plasma extravasation was transient and recovered soon after removal of the stressor.…”

“…Therefore, it seems unlikely that these transient actions would have noticeable effects on full-blown inflammatory disease, such as the aggravation of symptoms reported clinically (2-4). Transient inhibition of plasma extravasation during an acute stressor is mediated by the stress-activated sympathoadrenal axis (11) and may involve physiological changes (i.e., catechol-mediated increases in heart rate and blood pressure) that subside quickly after the stressor is removed.…”

Antidepressant and antistress activity of GC‐MS characterized lipophilic extracts of Ginkgo biloba leaves

“…The antistress activity was investigated by cold immobilization stress-induced gastric ulceration, after acute treatment in albino rats (Bhattacharya et al, 1987). Thus, rats were immobilized on wooden planks following the Freglys method of immobilization.…”

“…The severity of ulcer was then calculated and the ulcer index was determined by adding the number of ulcers as reported earlier (Bhattacharya et al, 1987).…”

Temporal study of carrageenan-induced PMN migration in mice

“…The presence of a 17.00 peak, when carrageenan is used in this experiment, supports the idea that antigens efficacy is more prominent during the early activity span of mice and that the circadian rhythm observed is independant of the type of antigen. It has been suggested that the sympatho-medullary system is responsible for an antiinflammatory effect rather than the release of adrenal corticoids [11]. These findings indicate that inflammation inhibition is a consequence of increased central noradrenergic and peripheral sympathomeduUary activity.…”