Sympathectomy. Unilateral removal of the SCG results in the reinnervation of the denervated cerebral vessel by sprouting nerves from the contralateral ganglion (Kahrstrom et al. 1986). Following chronic guanethidine sympathectomy there is a complete depletion of sympathetic cotransmitters NA and NPY from the dura mater but an increase in the expression of NPY in non-sympathetic axons (lacking small dense-cored vesicles) supplying cerebral vessels and the iris (Mione at al. 1990). The source of increased cerebrovasular NPY is thought to be preexisting parasympathetic cranial ganglia which normally express both NPY and VIP (Gibbins and Morris 1998).
Indeed, sympathectomy-induced DBH-immunoreactivity in the sphenopalatine (parasympathetic) ganglion occurs at the same time as a loss of VIP-immunoreactivity (Fan and Smith 1993). In the cerebral and uterine artery, loss of sympathetic nerves also leads to increased DBH-immunoreactivity in non-sympathetic nerves that lack TH and NA (Morris et al. 1991).
The loss of sympathtetic neurones and nerve fibres is also accompanied by striking increases in sensory innervation. This has been attributed to increased availability to NGF (as there are no sympathetic nerves with which to compete for uptake) which promotes the growth of sensory nerves (Kessler et al. 1983)
In the lung, sympathectomy induced a marked increase in CGRP-immunoreactive nerve density around the airways, and blood vessels.
Category: Neurology & Clinical Neurophysiology
Publication Date: 1999-12-16 Publisher: Elsevier - Health Sciences Div