Neurogenic and non-neurogenic inflammation in the rat paw following chemical sympathectomy.

Rats with chemical sympathectomy, induced either at neonatal age (long-term sympathectomy) or in adult animals (short-term sympathectomy) by guanethidine or by 6-hydroxydopamine, were used to determine the contribution of sympathetic noradrenergic fibres to afferent neuron-mediated responses and to non-neurogenic inflammation in the rat. Following long-term sympathectomy with 6-hydroxydopamine there was a 66% depletion of noradrenaline in the paw skin. This was accompanied by a 20-53% increase in the levels of sensory neuropeptides in the paw skin and sciatic nerve. A hypersensitivity towards heat stimuli was observed in the tail immersion test. Neither neurogenic plasma protein extravasation following antidromic nerve stimulation or upon local mustard oil application nor the development of the non-neurogenic carrageenan oedema and its susceptibility towards indomethacin were impaired. Neonatal guanethidine sympathectomy caused an 86% depletion of noradrenaline in the paw skin and neurogenic plasma protein extravasation upon antidromic nerve stimulation was impaired. Sensory neuropeptides were unchanged in the skin after neonatal guanethidine and only calcitonin gene-related peptide content was increased in the spinal cord and sciatic nerves. The other observations (i.e. the sensitivity towards heat stimuli, the neurogenic mustard oil inflammation and the non-neurogenic carrageenan oedema) were similar to those observed after neonatal 6-hydroxydopamine treatment. Following the short-term treatment protocol of 6-hydroxydopamine, an 82% depletion of noradrenaline in the skin was accompanied by an increase in calcitonin gene-related peptide content, whereas after adult guanethidine (60% depletion of noradrenaline) levels of sensory neuropeptides were unchanged. Neurogenic plasma protein extravasation was found to be unimpaired after either type of short-term chemical sympathectomy.(ABSTRACT TRUNCATED AT 250 WORDS)