Koltzenburg M, Häbler H J, Jänig W
Neurologische Universitäts-Klinik, Würzburg, Germany.
Neuroscience. 1995 Jul;67(1):245-52. doi: 10.1016/0306-4522(95)00033-f.
Sympathetic vasoconstrictor neurons that had previously innervated blood vessels in hairy skin were made to reinnervate the vasculature of the hairless skin of the paw pad by suturing the central stump of the cut sural nerve to the distal stump of the cut tibial nerve. After allowing sufficient time for the reinnervation, electrical stimulation of the vasoconstrictor pathway in the lumbar sympathetic trunk produced a reduction of the blood flow that was significantly greater than in control animals. There was also a clear sign of a "denervation supersensitivity" of the blood vessels as evidenced by a significantly increased vasoconstriction that followed the systemic application of the alpha 1-adrenoceptor specific agonist phenylephrine. Neurogenic vasodilation evoked by antidromic excitation of small diameter primary afferent neurones was significantly impaired although myelinated and unmyelinated primary afferents had re-grown into the target tissue. Electrical stimulation of the intact tibial nerve (containing sympathetic vasoconstrictor axons and nociceptive primary afferent fibres) in control animals, always produced vasodilatation indicating that the neurogenic vasodilatation can override the sympathetic vasoconstrictor response. By contrast, electrical stimulation of cross-unioned nerves consistently produced a robust vasoconstriction. We conclude that sympathetic vasoconstrictor neurons have a high capacity to functionally reinnervate autonomic effector organs in the adult cat. Despite this functional recovery, the blood vessels exhibited stronger than normal responses to an alpha 1-adrenoceptor agonist. The impaired neurogenic vasodilatation mediated by small diameter afferents may be due to their poor ability to re-establish their efferent vasodilatory function. Alternatively it may be masked by the strong vasoconstriction.
通过将切断的腓肠神经的中枢残端缝合到切断的胫神经的远侧残端，使先前支配多毛皮肤血管的交感缩血管神经元重新支配爪垫无毛皮肤的血管系统。在给予足够的时间进行神经再支配后，电刺激腰交感干中的缩血管通路，所产生的血流量减少显著大于对照动物。血管也有明显的“去神经超敏反应”迹象，这可通过全身应用α1-肾上腺素能受体特异性激动剂去氧肾上腺素后显著增强的血管收缩来证明。尽管有髓鞘和无髓鞘的初级传入神经已重新长入靶组织，但由小直径初级传入神经元的逆向兴奋引起的神经源性血管舒张仍明显受损。在对照动物中，电刺激完整的胫神经（包含交感缩血管轴突和伤害性初级传入纤维）总是产生血管舒张，这表明神经源性血管舒张可以克服交感缩血管反应。相比之下，交叉联合神经的电刺激始终产生强烈的血管收缩。我们得出结论，交感缩血管神经元在成年猫中有很高的能力对自主效应器官进行功能性再支配。尽管有这种功能恢复，但血管对α1-肾上腺素能受体激动剂的反应比正常情况更强。小直径传入神经介导的神经源性血管舒张受损可能是由于它们重新建立传出血管舒张功能的能力较差。或者，它可能被强烈的血管收缩所掩盖。
