1990 年 37 巻 SUPPLEMENT 号 p. S23-S32
The characteristic symtoms of vibration disease, such as Reynaud's phenomnon and palmar superhydrosis, are associeted with a sympathetic hyperactivity. This paper discusses the possible sites and mechanisms of the vibration stress-induced facilitation and disinhibition in the sympathetic nervous system, particularly at the levels of the spinal cord and sympathetic ganglion. At the level of the preganglionic neurons, vibration stress may facilitate the activity of the alpha-1 adrenoceptors that mediate the slow excitatory postsyn-aptic potential and the spike-afterdepolarization. If the sympathetic hyperactivity is in part due to disinhibition, it could be produced by inhibition of the activity of the alpha-2 adrenoceptors that mediate the slow inhibitory postsynaptic potential in preganglionic neurons. At the level of the ganglion, muscarinic and peptidergic tranmission may be facilitated in vibration disease.
