Nishi S
Department of Physiology, Kurume University School of Medicine, Japan.
Kurume Med J. 1990;37 Suppl:S23-32. doi: 10.2739/kurumemedj.37.supplement_s23.
The characteristic symptoms of vibration disease, such as Raynaud's phenomenon and palmar superhydrosis, are associated 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 postsynaptic potential and the spike-after depolarization. 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 transmission may be facilitated in vibration disease.
振动病的特征性症状，如雷诺现象和手掌多汗症，与交感神经功能亢进有关。本文讨论了振动应激在交感神经系统中诱导易化和去抑制作用的可能部位及机制，特别是在脊髓和交感神经节水平。在节前神经元水平，振动应激可能会促进介导缓慢兴奋性突触后电位和锋电位后去极化的α-1肾上腺素能受体的活性。如果交感神经功能亢进部分是由于去抑制作用引起的，那么它可能是由抑制介导节前神经元缓慢抑制性突触后电位的α-2肾上腺素能受体的活性所产生的。在神经节水平，毒蕈碱能和肽能传递在振动病中可能会得到促进。
