The effect of central and peripheral administration of acetylcholine and epinephrine on respiration.

The experiments were conducted in dogs anesthetized with Na-pentobarbital i.v. tidal volume (VT) and respiratory frequency (f min-1) were recorded. The central effects of acetylcholine (Ach) and epinephrine on respiration were investigated after injections of these substances directly into the cerebrospinal fluid by atlanto-occipital punction. The peripheral effects of Ach and epinephrine on respiration were studied after i.v. injections. Both central and peripheral administration of epinephrine caused significant increase in f min-1 and VT. After vagotomy the effects of centrally and peripherally administered epinephrine on f min-1 were abolished. The effect of central injection of epinephrine on VT persisted after vagotomy. The increase in VT in response to peripheral epinephrine administration was abolished by vagotomy. Both central and peripheral injection of Ach increased f min-1. In VT an initial decrease was followed by an increase. The initial decrease in VT was abolished by atropine. After vagotomy the effects of central and peripheral administration of Ach on f min-1 were abolished. The effects of central injection of Ach on VT persisted after vagotomy. Vagotomy abolished the effects of peripheral administration of Ach on VT.

Central noradrenergic and cholinergic modulation of formaldehyde-induced pedal inflammation and nociception in rats.

Possible central noradrenergic and cholinergic modulation of acute peripheral inflammation was investigated in rats, adopting the formaldehyde-induced pedal inflammation as the experimental model. Intracerebroventricularly (icv) administered noradrenaline (NA), alpha-adrenoceptor agonist, L-phenylephrine, alpha-2 adrenoceptor agonist, clonidine and non-selective beta-adrenoceptor blocker, propranolol, suppressed formaldehyde-induced inflammation producing a decrease in oedema volume and increase in pain threshold. Conversely, both noradrenergic neuron degenerator, 6-hydroxydopamine (6-OHDA) and non-selective alpha-adrenoceptor antagonist, phenoxybenzamine produced an increase in paw oedema along with an augmentation of pain. Significant oedema augmenting effects were also produced by central excitatory neurotransmitter, acetylcholine (ACh) on icv administration. ACh also produced pro-nociceptive action. An ACh antagonist, scopolamine and ACh synthesis inhibitor, hemicholinium-3 (HC) reduced pedal oedema and produced analgesia. The results of this study indicate that central NA exerts an inhibitory effect on peripheral oedema and pain whereas, ACh has an augmenting effect on formaldehyde-induced peripheral inflammation.